Diagnosis
A 12-lead ECG of a person with CKD and a severe electrolyte imbalance:
hyperkalemia (7.4 mmol/l) with hypocalcemia (1.6 mmol/l). The T-waves
are peaked and the QT interval is prolonged.
Diagnosis of CKD is largely based on the clinical picture combined with the measurement of the serum creatinine level .
Etiology
In many CKD patients, previous kidney disease or other underlying
diseases are already known. A significant number present with CKD of
unknown cause. In these patients, a cause is occasionally identified
retrospectively.[citation needed]
Differential diagnosis
It is important to differentiate CKD from acute kidney injury (AKI)
because AKI can be reversible. Abdominal ultrasound, in which the size
of the kidneys is measured, is commonly performed. Kidneys with CKD are
usually smaller (≤ 9 cm) than normal kidneys, with notable exceptions
such as in early diabetic nephropathy and polycystic kidney disease.
Another diagnostic clue that helps differentiate CKD from AKI is a
gradual rise in serum creatinine (over several months or years) as
opposed to a sudden increase in the serum creatinine (several days to
weeks). If these levels are unavailable (because the patient has been
well and has had no blood tests), it is occasionally necessary to treat a
patient briefly as having AKI until the kidney impairment has been
established to be irreversible.
Treatment
Controlling blood pressure will slow further kidney damage.
Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are used most often.
The goal is to keep blood pressure at or below 130/80 mmHg.
Making lifestyle changes can help protect the kidneys, and prevent heart disease and stroke, such as:
Do not smoke.
Eat meals that are low in fat and cholesterol.
Get regular exercise (talk to your doctor or nurse before starting to exercise).
Take drugs to lower your cholesterol, if needed.
Keep your blood sugar under control.
Avoid eating too much salt or potassium.
Always talk to your kidney doctor before taking any over-the-counter
medicine. This includes vitamins, herbs and supplements. Make sure all
of the doctors you visit know you have chronic kidney disease.
Other treatments may include:
Medicines called phosphate binders, to help prevent high phosphorous levels
Extra iron in the diet, iron pills, iron given through a vein
(intravenous iron) special shots of a medicine called erythropoietin,
and blood transfusions to treat anemia
Extra calcium and vitamin D (always talk to your doctor before taking)
Your doctor may have you follow a special diet for chronic kidney disease.
Limiting fluids
Eating less protein
Restricting salt, potassium, phosphorous, and other electrolytes
Getting enough calories to prevent weight loss
All people with chronic kidney disease should be up-to-date on the following vaccinations:
Hepatitis A vaccine
Hepatitis B vaccine
Flu vaccine
Pneumonia vaccine (PPV)
The treatment of traditional chinese medicine and chinese herbal
medicine . this therapy improve kidney blood circulation .Increase
glomerular filtration rate .so this therapy can stop and reverse the
progress of some patients with chronic renal failure .At stage 5ckd
renal replacement therapy is uaually in the form of either dialysis or a
transplant.
2015年11月30日星期一
2015年11月24日星期二
GFR is 44 and creatinine is 1.6
Question: I have Stage 3 CKD, and my GFR is 44 and creatinine is 1.6. Now, I don’t have other symptoms. Should I begin to take some treatments?
Answer: Both GFR and creatinine are two indicators of dividing Chronic Kidney Disease. Normally, patients can still live without obvious symptoms, when their glomerular filtration rate (GFR) is still about 50%. This is because our kidneys have strong compensatory ability that makes people live normally even if they donate one of their kidneys to other people. However, when GFR declines to below 50%, more and more waste products and toxins will build up in the blood that causes serum creatinine to increase. If left alone, GFR will reduce and creatinine level will increase quickly.
From the above analysis, we can know Stage 3 CKD is the best time to reverse kidney damage and improve kidney condition. Here, we have some methods that kidney patients can have a try.
- Traditional Chinese Medicine: As we know, Chinese medicines are good at treating chronic disease as well as kidney disease and regulating internal environment. Some Chinese medicines have the property of activating blood and nourishing damaged kidney cells, so they can help protect remaining kidney functioning cells and repairing damaged but not necrotic cells gradually.
- Micro-Chinese Medicine Hot Compress Therapy: This is one innovation of TCM that can make prescribed Chinese medicines work more quickly. Of course, some auxiliary treatments are also added into this therapy, such as, acupuncture, medicated bath, massage, etc. You can a lot of benefits from these therapies.
To know what medicines or methods you can use, please send email to anna.hospital@kididel.com or leave a message below.
2015年11月22日星期日
Sudden Decrease of Vision Cused by Uremia Seeking Treatment in Shijiazhuang Kidney Disease Hospital
When occurring to the sudden decrease of vision and blurred vision, the first reaction of most people is to do an eye examination. However, there are also such patients in nephrology department. The reporter learned that the sudden decrease of vision may has a strong relationship with kidney health.
The 23 years old boy La Zhu from south area of Tibet dropped out of school since senior two because of the poverty of his family. Half a year ago, he found there is something wrong with his eyes.He couldn’t see well and getting more and more blurred.
“ It’s strange. I don’t go to school for many years so neither overuse my eyes nor myopia. Can’t be presbyopia?”La Zhu recalled.
With confusion, La Zhu went to many hospitals in Beijing to check his eyes but couldn’t find out the reason. Under the doctor’s suggestions, he went to nephrology department to check his condition. After checking, the result startled him. He was diagnosed with uremia combined with high blood pressure. Then La Zhu undergo dialysis.
It is not effective after three months of treatment. La Zhu doubt that uremia can lead to the blurred vision. So he went to Shijiazhuang kidney disease hospital and check again. However the experts from this hospital gave the same results. The expert told him that blurred vision is the early manifestation of uremia and suggested La Zhu to adopt the traditional Chinese medicine.
According to the introduction from Liu Lipei, La Zhu’s attending doctor, the reason why uremia can lead to the blurred vision is the toxins in kidney cause the damage to every organ of body. It can affect the retina and lead to the blurred vision. When the condition getting worse, it can make the patient blind. Uremic patient with high blood pressure can affect the retina and lead to the blurred vision.
“Most of our patients don’t know the reasons when they occurring to these symptoms, so they do eye examination to check their eyes first, therefore, it become an important reason for missing the best occasion for the treatment.” Liu Lipei says. When we find ourselves appearing the blurred vision with high blood pressure, we must check our renal function and avoid more harmful case.
“Luckily, when he find the true reason, he just stand the initial stage of uremia. He adopted the therapy timely and used the traditional Chinese medicine therapy to clear the poison in blood. It is effective and the condition is under control soon. Otherwise, there are too much toxins in his body, it may be more serious.” Liu Lipei says. Now the condition of La Zhu is under control and get rid of dialysis gradually.
Kidney disease has been called “invisible killer”. Because symptoms are not obvious at the very start. How can we discover the kidney disease in time through our body’s signals? Liu Lipei says, it is not easy to find at the beginning. There are no obvious manifestations in early stage. However if you notice that the urine turns red and thick, you should pay more attention. Especially you appeared cold and diarrhea, the urine turning red, it may relate to IgA nephropathy post infection.
Eight Cups of Water Can Preserve One's Health
Professors Said: Water, Over 3000 Milligrams Can Damage Kidney.
The news report of“5-year-old boy punished to drink 20 cups water
lead to hydronephrosis”caused heated debate by many net friends. It can
cause hydronephrosis after a lot of water intake? If the saying of‘’8
cups of water in daily‘’regarded as principle by many people is reliable
?Too much water brings us health or damage?In Shijiazhuang Kidney Disease Hospital , journalists know about that drinking water should follow “water intake equals water output”rule. Plain boiled water is the main and best, and can’t drink too much for only one time. Moreover ,never drink water only get thirsty ,and drink a little but many times is the best way and the effect will be the best.
Excess water intake can cause poisoning.
Adults consume 2500ml water daily, which is not only the water we drink but the water in the food, such as vegetables, in which 90% is water, and fruits ,in which 80% is water.
It maybe too much to intake 3000ml water everyday and it is especially too much for patients with bad heart and kidney function, or patients with pumonary resection and kidney function problems.
Thus ,moderate water drinking can benefit your body, but too much water not only have no benefit but also can damage your body, even lead to poisoning.
Where does the criterion come from?
The saying of eight cups of water is very general. Some people regard 150ml cup as a cup, but there are also people regarding 220ml,250ml and big cup of 500ml a cup, which make the water intake differ a lot.
From a scientific point of view, it is not a wise behavior to insist on the criterion, even it maybe harmer than good.
Then, where does the 8 cups water criterion comes from? Shiwei indicated that there was no people know the criterion origin.
Too much mineral content is not good.
Many people think that the purer the water is, the better it is, but actually ,long-term Clearwater drinking can lead to body malnutrition. Long-term Clearwater drinking can take away the useful microelement ,and then lower the body immunity and easy to cause disease.
It’s known that scientists all think that good water intake should conforms with the following :
No pathogenic bacteria, heavy metal and harmful chemical substances; Contain moderate mineral substance and microelement; Contain moderate fresh dissolved Oxygen; More alkaline, and the molecular group should be small and active.
A great deal of water can lower the kidney filtration ability.
Eight-cup-water’s cosmetic result which has become a hit on the internet ,not only be chased after by young women, but also many old people all think that a lot of daily water intake can eliminate the body toxin. In the dog days, there are many people even think the water intake should be more than 3000ml for eliminating the body toxin.
According to what Shiwei said, the kidney filtrates our toxin in the blood circulation ,and then the toxin is secreted through urine. But, actually ,drinking too much water can decrease the kidney filtration ability which is very tiny but really exists.
Scientific drinking time
In the morning, drink water moderate water after getting up can replenish the water consumed in the nighttime.
Drinking water, about 1 hour before the three meals, can make the water into histocytes of the whole body, satisfied the water need of the body, ensure the necessary and enough digestive juice to increase the appetite and help the body digest and absorb.
Drinking in the working time can supplement the water which is secreted in working and eliminated through urine, and the waste staying in the body also can be easily secreted owing to the water drinking. It can increase the feeling of fullness to drink a cup of water before leaving the office.
Two to three hour before sleeping drinking water can dilute the blood and stimulate the blood circulation.
2015年11月21日星期六
renal anemia -risk factor for chronic kidney disease
Discussion
Anemia ia associated with a more severe impairment of renal function
in this study and other published research.Anemia severity correlates
with thre degree of renal function impairment an there is evidence that
low levels of Hb were associated with accelerated progression of CKD
.Introduction of EPO in therapy to these patients
Reduce transfusion requirements and improve quality of life of these patients .In our study EPO administration resulted in improved GFR in patients with anemia and there are other studies that reporting an improvement in GFR in patients with anemia and there are other studies that reporting an impronement in GFR decline after correcting anemia ith EPO.According with other published data .there was no difference in the progression rate of CKD in patients with higher values of Hb after EPO use，but was a higher rate of adverse events such as myocardial infarction,death ,hospitalization .In our study GFR was higher in patients without disables and without anemia ompared with those who had anemia and diabetes,too.There are other published research which shows that the association of anemia and DM in patients with CKD had been shown to accelerate the progression of CKD, increasing cardiovascular morbidity and mortality ,in association with a poor prognosis of these patients , Anemia associated inflammation contributes to the decline in GFR , anemia secondary to hypoxia , casuaing inflammation and fibrosis and loss of capillaries , In this study , anemia accompanied by inflammation was associated with a significantly higher risk of developing severe renal impairment . Secondary hyperparathyroidism is associated with hyporesponsiveness to EPO therapy and vitamin D deficiency was associated with reduced hemoglobin levels in patients with CKD . In our study the association of anemia with secondary HPT led to a significant decline in GFR within 12 months of morning . The presence of anemia was associated with a greater number of days of hospitalization (p=0.0001) . In a retrospective study demonstrated that patients with low Hb levels had the highest rate of hospitalization and several comorbidities.
Conclusions
Anemia , a frequent feature of CKD , play an important role in progression of renal impairment ,probably due to hypoxia ,especially in combination with other risk factors such as diabetes or inflammation . Thus early identification and correction of anemia is important for slowing the progression of CKD.
Abbreviation
Hb=hemoglobin
OM=diabetes mellitus
CKD=chronic kidney disase
GFR=glomcrular filtration rate
HPT=hyperparathyroidism
EPO=erythropoietin
Reduce transfusion requirements and improve quality of life of these patients .In our study EPO administration resulted in improved GFR in patients with anemia and there are other studies that reporting an improvement in GFR in patients with anemia and there are other studies that reporting an impronement in GFR decline after correcting anemia ith EPO.According with other published data .there was no difference in the progression rate of CKD in patients with higher values of Hb after EPO use，but was a higher rate of adverse events such as myocardial infarction,death ,hospitalization .In our study GFR was higher in patients without disables and without anemia ompared with those who had anemia and diabetes,too.There are other published research which shows that the association of anemia and DM in patients with CKD had been shown to accelerate the progression of CKD, increasing cardiovascular morbidity and mortality ,in association with a poor prognosis of these patients , Anemia associated inflammation contributes to the decline in GFR , anemia secondary to hypoxia , casuaing inflammation and fibrosis and loss of capillaries , In this study , anemia accompanied by inflammation was associated with a significantly higher risk of developing severe renal impairment . Secondary hyperparathyroidism is associated with hyporesponsiveness to EPO therapy and vitamin D deficiency was associated with reduced hemoglobin levels in patients with CKD . In our study the association of anemia with secondary HPT led to a significant decline in GFR within 12 months of morning . The presence of anemia was associated with a greater number of days of hospitalization (p=0.0001) . In a retrospective study demonstrated that patients with low Hb levels had the highest rate of hospitalization and several comorbidities.
Conclusions
Anemia , a frequent feature of CKD , play an important role in progression of renal impairment ,probably due to hypoxia ,especially in combination with other risk factors such as diabetes or inflammation . Thus early identification and correction of anemia is important for slowing the progression of CKD.
Abbreviation
Hb=hemoglobin
OM=diabetes mellitus
CKD=chronic kidney disase
GFR=glomcrular filtration rate
HPT=hyperparathyroidism
EPO=erythropoietin
2015年11月17日星期二
Acute Renal Failure (ARF)
Acute kidney injury (AKI), previously called acute renal failure (ARF),is an abrupt loss of kidney function that develops within 7 days.
Its causes are numerous. Generally it occurs because of damage to the kidney tissue caused by decreased renal blood flow (renal ischemia) from any cause (e.g. low blood pressure), exposure to substances harmful to the kidney, an inflammatory process in the kidney, or an obstruction of the urinary tract which impedes the flow of urine. AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine, or inability of the kidneys to produce sufficient amounts of urine.
AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, and effects on other organ systems, including death. People who have experienced AKI may have an increased risk of chronic kidney disease in the future. Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy.
Signs and symptoms
The clinical picture is often dominated by the underlying cause, eg postoperative state. The symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue, loss of appetite, headache, nausea and vomiting.Marked increases in the potassium level can lead to irregularities in the heartbeat, which can be severe and life-threatening.Fluid balance is frequently affected, though blood pressure can be high, low or normal.
Pain in the flanks may be encountered in some conditions (such as thrombosis of the renal blood vessels or inflammation of the kidney); this is the result of stretching of the fibrous tissue capsule surrounding the kidney.If the kidney injury is the result of dehydration, there may be thirst as well as evidence of fluid depletion on physical examination.Physical examination may also provide other clues as to the underlying cause of the kidney problem, such as a rash in interstitial nephritis (or vasculitis) and a palpable bladder in obstructive nephropathy.
Causes
AKI can be caused by systemic disease (such as a manifestation of an autoimmune disease, e.g. lupus nephritis), crush injury, contrast agents, some antibiotics, and more. It is often multifactorial. The most common cause is dehydration and sepsis combined with nephrotoxic drugs, especially following surgery or contrast agents.
The causes of acute kidney injury are commonly categorized into prerenal, intrinsic, and postrenal.
Classic laboratory findings in AKI
Type UOsm UNa FeNa BUN/Cr
Prerenal >500 <10 <1% >20
Intrinsic <350 >20 >2% <15[citation needed]
Postrenal <350 >40 >4% >15
Prerenal
Prerenal causes of AKI ("pre-renal azotemia") are those that decrease effective blood flow to the kidney. These include systemic causes, such as low blood volume, low blood pressure, heart failure, liver cirrhosis and local changes to the blood vessels supplying the kidney. The latter include renal artery stenosis, or the narrowing of the renal artery which supplies the kidney with blood, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney.
Renal ischaemia can result in depression of GFR. Causes include inadequate cardiac output and hypovolemia or vascular diseases causing reduced perfusion of both kidneys. Both kidneys need to be affected as one kidney is still more than adequate for normal kidney function.
Intrinsic
Sources of damage to the kidney itself are dubbed intrinsic. Intrinsic AKI can be due to damage to the glomeruli, renal tubules, or interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively. Other causes of intrinsic AKI are rhabdomyolysis and tumor lysis syndrome.
Postrenal
Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, obstructed urinary catheter, bladder stone, bladder, ureteral or renal malignancy. It is useful to perform a bladder scan or a post void residual to rule out urinary retention. In post void residual, a catheter is inserted immediately after urinating to measure fluid still in the bladder. 50-100 ml suggests neurogenic bladder dysfunction. A renal ultrasound will demonstrate hydronephrosis if present. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis. However, in AKI, the use of IV contrast is contraindicated as the contrast agent used is nephrotoxic. On the basic metabolic panel, the ratio of BUN to creatinine may indicate post renal failure.
Diagnosis
Detection
The deterioration of renal function may be discovered by a measured decrease in urine output. Often, it is diagnosed on the basis of blood tests for substances normally eliminated by the kidney: urea and creatinine. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers has been proposed (such as NGAL, KIM-1, IL18 and cystatin C), but none are currently established enough to replace creatinine as a marker of renal function.Use of the renal angina index, a composite of risk factors and early signs of injury, has been used to detect fulfillment of renal angina in children.
Further testing
Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. These may include urine sediment analysis, renal ultrasound and/or renal biopsy. Indications for renal biopsy in the setting of AKI include:
Unexplained AKI, in a patient with two non-obstructed normal sized kidneys
AKI in the presence of the nephritic syndrome
Systemic disease associated with AKI
Renal transplant dysfunction
Classification
Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria (less than 400 mls of urine per 24 hours).
Definition
Introduced by the KDIGO in 2012,specific criteria exist for the diagnosis of AKI.
AKI can be diagnosed if any one of the following is present:
Increase in SCr by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or
Increase in SCr to ≥1.5 times baseline, which have occurred within the prior 7 days; or
Urine volume < 0.5 ml/kg/h for 6 hours.
Staging
The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in the staging of patients with AKI:
Risk: 1.5-fold increase in the serum creatinine, or glomerular filtration rate (GFR) decrease by 25 percent, or urine output <0.5 mL/kg per hour for six hours.
Injury: Two-fold increase in the serum creatinine, or GFR decrease by 50 percent, or urine output <0.5 mL/kg per hour for 12 hours
Failure: Three-fold increase in the serum creatinine, or GFR decrease by 75 percent, or urine output of <0.3 mL/kg per hour for 24 hours, or anuria for 12 hours
Loss: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than four weeks
End-stage renal disease: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than three months
Treatment
The management of AKI hinges on identification and treatment of the underlying cause. The main objectives of initial management are: (1) to prevent cardiovascular collapse and death; and, (2) to call for specialist advice. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances.
Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.
Specific therapies
In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improve renal function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid.
Should low blood pressure prove a persistent problem in the fluid-replete patient, inotropes such as norepinephrine and dobutamine may be given to improve cardiac output and hence renal perfusion. While a useful pressor, there is no evidence to suggest that dopamine is of any specific benefit,and may be harmful.
The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to vasculitis or glomerulonephritis may respond to steroid medication, cyclosphosphamide and (in some cases) plasma exchange. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as ACE inhibitors, ARB antagonists, aminoglycosides, penicillins, NSAIDs, or paracetamol.
If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.
Diuretic agents
The use of diuretics such as furosemide, is widespread and sometimes convenient in ameliorating fluid overload. It is not associated with higher mortality (risk of death),nor with any reduced mortality or length of intensive care unit or hospital stay.
Renal replacement therapy
Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI. A systematic review of the literature in 2008 demonstrated no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration (CVVH).Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis.
Its causes are numerous. Generally it occurs because of damage to the kidney tissue caused by decreased renal blood flow (renal ischemia) from any cause (e.g. low blood pressure), exposure to substances harmful to the kidney, an inflammatory process in the kidney, or an obstruction of the urinary tract which impedes the flow of urine. AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine, or inability of the kidneys to produce sufficient amounts of urine.
AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, and effects on other organ systems, including death. People who have experienced AKI may have an increased risk of chronic kidney disease in the future. Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy.
Signs and symptoms
The clinical picture is often dominated by the underlying cause, eg postoperative state. The symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue, loss of appetite, headache, nausea and vomiting.Marked increases in the potassium level can lead to irregularities in the heartbeat, which can be severe and life-threatening.Fluid balance is frequently affected, though blood pressure can be high, low or normal.
Pain in the flanks may be encountered in some conditions (such as thrombosis of the renal blood vessels or inflammation of the kidney); this is the result of stretching of the fibrous tissue capsule surrounding the kidney.If the kidney injury is the result of dehydration, there may be thirst as well as evidence of fluid depletion on physical examination.Physical examination may also provide other clues as to the underlying cause of the kidney problem, such as a rash in interstitial nephritis (or vasculitis) and a palpable bladder in obstructive nephropathy.
Causes
AKI can be caused by systemic disease (such as a manifestation of an autoimmune disease, e.g. lupus nephritis), crush injury, contrast agents, some antibiotics, and more. It is often multifactorial. The most common cause is dehydration and sepsis combined with nephrotoxic drugs, especially following surgery or contrast agents.
The causes of acute kidney injury are commonly categorized into prerenal, intrinsic, and postrenal.
Classic laboratory findings in AKI
Type UOsm UNa FeNa BUN/Cr
Prerenal >500 <10 <1% >20
Intrinsic <350 >20 >2% <15[citation needed]
Postrenal <350 >40 >4% >15
Prerenal
Prerenal causes of AKI ("pre-renal azotemia") are those that decrease effective blood flow to the kidney. These include systemic causes, such as low blood volume, low blood pressure, heart failure, liver cirrhosis and local changes to the blood vessels supplying the kidney. The latter include renal artery stenosis, or the narrowing of the renal artery which supplies the kidney with blood, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney.
Renal ischaemia can result in depression of GFR. Causes include inadequate cardiac output and hypovolemia or vascular diseases causing reduced perfusion of both kidneys. Both kidneys need to be affected as one kidney is still more than adequate for normal kidney function.
Intrinsic
Sources of damage to the kidney itself are dubbed intrinsic. Intrinsic AKI can be due to damage to the glomeruli, renal tubules, or interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively. Other causes of intrinsic AKI are rhabdomyolysis and tumor lysis syndrome.
Postrenal
Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, obstructed urinary catheter, bladder stone, bladder, ureteral or renal malignancy. It is useful to perform a bladder scan or a post void residual to rule out urinary retention. In post void residual, a catheter is inserted immediately after urinating to measure fluid still in the bladder. 50-100 ml suggests neurogenic bladder dysfunction. A renal ultrasound will demonstrate hydronephrosis if present. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis. However, in AKI, the use of IV contrast is contraindicated as the contrast agent used is nephrotoxic. On the basic metabolic panel, the ratio of BUN to creatinine may indicate post renal failure.
Diagnosis
Detection
The deterioration of renal function may be discovered by a measured decrease in urine output. Often, it is diagnosed on the basis of blood tests for substances normally eliminated by the kidney: urea and creatinine. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers has been proposed (such as NGAL, KIM-1, IL18 and cystatin C), but none are currently established enough to replace creatinine as a marker of renal function.Use of the renal angina index, a composite of risk factors and early signs of injury, has been used to detect fulfillment of renal angina in children.
Further testing
Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. These may include urine sediment analysis, renal ultrasound and/or renal biopsy. Indications for renal biopsy in the setting of AKI include:
Unexplained AKI, in a patient with two non-obstructed normal sized kidneys
AKI in the presence of the nephritic syndrome
Systemic disease associated with AKI
Renal transplant dysfunction
Classification
Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria (less than 400 mls of urine per 24 hours).
Definition
Introduced by the KDIGO in 2012,specific criteria exist for the diagnosis of AKI.
AKI can be diagnosed if any one of the following is present:
Increase in SCr by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or
Increase in SCr to ≥1.5 times baseline, which have occurred within the prior 7 days; or
Urine volume < 0.5 ml/kg/h for 6 hours.
Staging
The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in the staging of patients with AKI:
Risk: 1.5-fold increase in the serum creatinine, or glomerular filtration rate (GFR) decrease by 25 percent, or urine output <0.5 mL/kg per hour for six hours.
Injury: Two-fold increase in the serum creatinine, or GFR decrease by 50 percent, or urine output <0.5 mL/kg per hour for 12 hours
Failure: Three-fold increase in the serum creatinine, or GFR decrease by 75 percent, or urine output of <0.3 mL/kg per hour for 24 hours, or anuria for 12 hours
Loss: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than four weeks
End-stage renal disease: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than three months
Treatment
The management of AKI hinges on identification and treatment of the underlying cause. The main objectives of initial management are: (1) to prevent cardiovascular collapse and death; and, (2) to call for specialist advice. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances.
Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.
Specific therapies
In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improve renal function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid.
Should low blood pressure prove a persistent problem in the fluid-replete patient, inotropes such as norepinephrine and dobutamine may be given to improve cardiac output and hence renal perfusion. While a useful pressor, there is no evidence to suggest that dopamine is of any specific benefit,and may be harmful.
The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to vasculitis or glomerulonephritis may respond to steroid medication, cyclosphosphamide and (in some cases) plasma exchange. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as ACE inhibitors, ARB antagonists, aminoglycosides, penicillins, NSAIDs, or paracetamol.
If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.
Diuretic agents
The use of diuretics such as furosemide, is widespread and sometimes convenient in ameliorating fluid overload. It is not associated with higher mortality (risk of death),nor with any reduced mortality or length of intensive care unit or hospital stay.
Renal replacement therapy
Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI. A systematic review of the literature in 2008 demonstrated no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration (CVVH).Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis.
2015年11月15日星期日
The Doctor in Shijiazhuang Kidney Disease Hospital wisely use the tips from Sudanese patient
“Dear Miss. Fatumi, I really surprised by your present, however it is my responsibility to take care of your father, I have already put that money (the present she gave to the doctor) in the hospital Finance department, which will be used for your father’s subsequent treatment ” Dr. Xiaohong Li, who from Shijiazhuang Kidney Disease Hospital International Department, told Miss. Fatumi, who from Sudan, by Whatsapp.
Mr. Muslifa is a dentist, 62 years old, and he has been suffering from Chronic Interstitial Nephritis for over 12 years, he came to Shijiazhuang kidney Disease Hospital one month ago to receive the Traditional Chinese Blood Purification Therapy, accompanied by her doctor.
After careful treatment, his condition get great improvement, so her doctor agreed him to discharge. Miss. Fatumi secretly gave Dr. Li a small box just when Dr, li escort them to the boarding gate in the airport, Miss Fatumi told Dr. Li :”Actually this gift is from my father, I am just on his behalf, Please do not open it until you go back, there will be a surprise”.
“To be honest, it was just a small box, I did not think too much, because when the foreign patients discharge, we will exchange some small gifts with national characteristic as souvenirs” Dr. Li said. “But when I opened the box, there was 300 USD cash folded into heart shape ”
Before Mr. Muslifa came to China, he was treated by Sudanese doctor, his doctor just told him to follow the diet, even though sometimes his condition become worse, but it was tolerable, because which did not affect his work and life at that time. However, he got a flu four months ago which made his condition aggravated. At that time, his creatinine level already reached to 1500umol/L, which was a really high level for Kidney disease patient. So the local doctor arranged him to do dialysis, because of the inadequate dialysis in the local hospital, his condition did not under control after 3 months treatment. Miss Fatumi works in a foreign trade business company, she really wanted to take his father to China for Traditional Chinese Medicine treatment, because she knows many Chinese people who study and work in Sudan, what’s more there are a lot of China Construction Aid Projects in Sudan, so Miss. Fatumi realized how amazing the Traditional Chinese Medicine is. Dr. Li said.
“During Mr. Muslifa hospitalization, her daughter needed to go back to her country because of her job, so during her absence, we took good care of her father , including treatment, casual talking, going shopping and so on ” “when he stayed here, he insisted to give tips many times, but we refused politely”. Dr Li said.
He found a dental clinic when we went shopping, Because Mr. Muslifa is a dentist, so he was interested in some tooth tools, he decided to buy some when he went back. When Dr. Li got to know the idea of Mr. Muslifa, she ordered the same tooth tools on the internet, additionally when Dr. Li was off duty, she bought some daily necessities like eye drops for him. Dr. Li thought that maybe because she did some extra work for him, so he offered her tips many times.
“The patient interests can not be violated, extra income are not allowed, that is the top prohibitions of our hospital, so we will refuse the tips, red envelope, and expensive gifts ” the Hospital president, Mr. Shi wei, said. Few years ago, some patients wanted to give bonuses to the doctors, but we refused gently, however, many patients thought that maybe their bonuses was less, which was the reason of doctors’ refusal, so they added more money, but the doctors still declined. What’s worse, which will lead to the negative mood of the patients, because they thought that their condition is serious, and the doctor afraid that they will fail to treat them, so they refuse the bonuses they gave to the doctors. So it will take time for the patients to accept this phenomenon of our hospital.
In order to let the patients receive the treatment without any unnecessary worries, we will put the bonuses which can not be refused to the hospital finance department, when the patient discharged, we will show the bill to the patient. Mr. Shi wei said that”some foreign patients will pay tips when they already in the airport, all the doctors refused, but because of the different culture, they thought the doctors do not like them or they have impolite behaviors in China which make people unhappy, so even when they went back, they would message the doctor , “did I do something wrong in China, ” so if we really can not refuse this bonus, we will put the money in the hospital finance department for patient subsequent treatment just exactly like what Dr. Li did.
When Mr. Fatumi came to know what Dr. Li did, she told this incredible story to other foreign patients who are still receiving the treatment in Shijiazhuang Kidney Disease Hospital, even though she maybe do not understand why Dr. Li did this. Mr. Lana, who is a PKD patient from Parkistan, he told Dr. Li by whatsapp :“you are awesome .”
2015年11月13日星期五
Etiology and Outcome of Crescentic Glomerulonephritis
Crescentic GN
remains one of the leading histologic diagnoss associated with acute or
rapidly progressive kidney failure.There is a paucity of reports from
China and few seriws from other parts of the world.We previously
analyzed data from 172 Chinese patients with crescentic GN to
characterize the clinical spectrum of crescentic GN during 1989 to
2001;however,the sample was small and clinicopathologic information was
limited.This report provodes more extensive and detailed information
about the occurrence and outcome of biopsy-diagnosed crescentic GN 33747
nontransplant-related biopsies performed during the past 10 years in
the biggest renal center in China.
Crescents can occur with most forms of primary GN and also are asociated with various systemic diseases.Among 33747 kidney biopsies was IGA nephritis and the mostprevalent secondary glomerular discase was lupus nephritis.Of note,in the present study,we also observed a limited number of instances of crescents associated with unusual disease entities,such as light-chain kidney disease,Alport syndrome,membranous nephropathy,focal segmental glomerulosclerosis,diabetic nephritis,and minimal change disease.These biopsy specimens had various percentage of crescents,usually with <50% of glomeruli having crescents,thus highlighting the need for considering these diseases as a cause of GN with crescents with decreased eGFR and the importance of performing an early kidney biopsy for accurate diagnosis and appropriate therapeutic decisions.
The spectrum of crescentic GN varied substantially among groups stratified by age and sex.Similar to previous reports,patients with anti-GBM disease(type I crescentic GN) were mainly middle-aged men with worse prognoses,and most had oliguria or hemoptysis and extensive glomerular crescent formation pathologically.Patients with immune complex-mediated crescentic GN(type II) were mainly young or middle-aged women and many had nephrotic syndrome,but nevertheless they showed good response to intensive immunosuppressive therapy.Patients with auci-immune crescentic GN(type III) were mainly middle-aged or elderly with multisystem involvement and had a relatively good response to intensive immunosuppressive therapy.
Almost half the patients in our cohort had AKI as their clinical presrntation,but it was remarkable that clinical presentation also included AKD in 13.1% and CKD in 28.8%,which were most commonly seen in patients with type II crescentic GN.Therefore,timely kidney biopsy should be emphasized for patients with decreased eGFRs,asymptomatic urinary abnormalities,and nephrotic syndrome without kidney atrophy in a kidney ultrasound to facilitate early diagnosis and proper treatment.
In pathologic findingd,mean proportions of glomeruli showing crescents were 80.6% in anti-GBM disease,63.1% in immune complex-mediated GN,and 73.2% in pauci-immune GN;crescents involving >80% glomeruli were seen in 55.7%,14.5%,and 39.0% of the 3 types,respectively.Proportions of cellular crescents,and fibrocellular crescents were similar among the 3 groups.
In conclusion, lupus nephritis may be the most common type of crescentic GN in china.and anti-GBM disease and pauci-immune crescentic GN are not rare in china. Clinical manifestations and outcomes vary by cresentic GN type.the distinction between vary by subtypes based on immunofluorescence and serologic findings has important implicationsfor therapy and outcome. We believe that the treatment of traditional chinese medicine combined with western medicine for crescentic GN ,is a kind of good method.
Crescents can occur with most forms of primary GN and also are asociated with various systemic diseases.Among 33747 kidney biopsies was IGA nephritis and the mostprevalent secondary glomerular discase was lupus nephritis.Of note,in the present study,we also observed a limited number of instances of crescents associated with unusual disease entities,such as light-chain kidney disease,Alport syndrome,membranous nephropathy,focal segmental glomerulosclerosis,diabetic nephritis,and minimal change disease.These biopsy specimens had various percentage of crescents,usually with <50% of glomeruli having crescents,thus highlighting the need for considering these diseases as a cause of GN with crescents with decreased eGFR and the importance of performing an early kidney biopsy for accurate diagnosis and appropriate therapeutic decisions.
The spectrum of crescentic GN varied substantially among groups stratified by age and sex.Similar to previous reports,patients with anti-GBM disease(type I crescentic GN) were mainly middle-aged men with worse prognoses,and most had oliguria or hemoptysis and extensive glomerular crescent formation pathologically.Patients with immune complex-mediated crescentic GN(type II) were mainly young or middle-aged women and many had nephrotic syndrome,but nevertheless they showed good response to intensive immunosuppressive therapy.Patients with auci-immune crescentic GN(type III) were mainly middle-aged or elderly with multisystem involvement and had a relatively good response to intensive immunosuppressive therapy.
Almost half the patients in our cohort had AKI as their clinical presrntation,but it was remarkable that clinical presentation also included AKD in 13.1% and CKD in 28.8%,which were most commonly seen in patients with type II crescentic GN.Therefore,timely kidney biopsy should be emphasized for patients with decreased eGFRs,asymptomatic urinary abnormalities,and nephrotic syndrome without kidney atrophy in a kidney ultrasound to facilitate early diagnosis and proper treatment.
In pathologic findingd,mean proportions of glomeruli showing crescents were 80.6% in anti-GBM disease,63.1% in immune complex-mediated GN,and 73.2% in pauci-immune GN;crescents involving >80% glomeruli were seen in 55.7%,14.5%,and 39.0% of the 3 types,respectively.Proportions of cellular crescents,and fibrocellular crescents were similar among the 3 groups.
In conclusion, lupus nephritis may be the most common type of crescentic GN in china.and anti-GBM disease and pauci-immune crescentic GN are not rare in china. Clinical manifestations and outcomes vary by cresentic GN type.the distinction between vary by subtypes based on immunofluorescence and serologic findings has important implicationsfor therapy and outcome. We believe that the treatment of traditional chinese medicine combined with western medicine for crescentic GN ,is a kind of good method.
2015年11月11日星期三
2015年11月9日星期一
Rapidly progressive glomerulonephritis
Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of renal function,(usually a 50% decline in the glomerular filtration rate (GFR) within 3 months) with glomerular crescent formation seen in at least 50% or 75% of glomeruli seen on kidney biopsies. If left untreated, it rapidly progresses into acute renal failure and death within months. In 50% of cases, RPGN is associated with an underlying disease such as Goodpasture syndrome, systemic lupus erythematosus, or granulomatosis with polyangiitis; the remaining cases are idiopathic. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents (crescent-shaped scars).
Signs and symptoms
Most types of RPGN are characterized by severe and rapid loss of kidney function featuring severe hematuria (blood in the urine), red blood cell casts in the urine, and proteinuria (protein in the urine), sometimes exceeding 3 g protein/24 h, a range associated with nephrotic syndrome. Some patients also experience hypertension (high blood pressure) and edema. Severe disease is characterized by pronounced oliguria or anuria, which portends a poor prognosis.
Most types of RPGN are characterized by severe and rapid loss of kidney function featuring severe hematuria (blood in the urine), red blood cell casts in the urine, and proteinuria (protein in the urine), sometimes exceeding 3 g protein/24 h, a range associated with nephrotic syndrome. Some patients also experience hypertension (high blood pressure) and edema. Severe disease is characterized by pronounced oliguria or anuria, which portends a poor prognosis.
Classification
Crescentic glomerulonephritis
RPGN can be classified into three types, based upon the immunofluorescence patterns:
RPGN can be classified into three types, based upon the immunofluorescence patterns:
Type I
Accounting for approximately 20% of RPGN, type I RPGN is characterized by the presence of autoantibodies directed against the glomerular basement membrane (GBM). It is also called anti-GBM glomerulonephritis. The antibodies are directed against a particular protein found in the GBM, type IV collagen, specifically the noncollagenous region of its α3 chain.In addition to the anti-GBM antibodies, some cases of type I RPGN are also associated with antibodies directed against the basement membrane of lung alveoli, producing Goodpasture syndrome. The majority of type I disease, however, features anti-GBM antibodies alone; these cases are considered idiopathic.
Accounting for approximately 20% of RPGN, type I RPGN is characterized by the presence of autoantibodies directed against the glomerular basement membrane (GBM). It is also called anti-GBM glomerulonephritis. The antibodies are directed against a particular protein found in the GBM, type IV collagen, specifically the noncollagenous region of its α3 chain.In addition to the anti-GBM antibodies, some cases of type I RPGN are also associated with antibodies directed against the basement membrane of lung alveoli, producing Goodpasture syndrome. The majority of type I disease, however, features anti-GBM antibodies alone; these cases are considered idiopathic.
Type II
RPGN caused by the deposition of immune complexes accounts for 25% of RPGN and is classified as type II. Thus any immune complex disease that involves the glomerulus may progress to RPGN if severe enough. These diseases include systemic lupus erythematosus, acute proliferative glomerulonephritis, Henoch-Schönlein purpura, and IgA nephropathy.
RPGN caused by the deposition of immune complexes accounts for 25% of RPGN and is classified as type II. Thus any immune complex disease that involves the glomerulus may progress to RPGN if severe enough. These diseases include systemic lupus erythematosus, acute proliferative glomerulonephritis, Henoch-Schönlein purpura, and IgA nephropathy.
Type III
Also known as pauci-immune RPGN, type III RPGN accounts for 55% of RPGN and features neither immune complex deposition nor anti-GBM antibodies. Instead, the glomeruli are damaged in an undefined manner, perhaps through the activation of neutrophils in response to ANCA. Type III RPGN may be isolated to the glomerulus (primary, or idiopathic) or associated with a systemic disease (secondary). In most cases of the latter, the systemic disease is an ANCA-associated vasculitis such as Wegener granulomatosis, microscopic polyangiitis, or Churg-Strauss syndrome.
Also known as pauci-immune RPGN, type III RPGN accounts for 55% of RPGN and features neither immune complex deposition nor anti-GBM antibodies. Instead, the glomeruli are damaged in an undefined manner, perhaps through the activation of neutrophils in response to ANCA. Type III RPGN may be isolated to the glomerulus (primary, or idiopathic) or associated with a systemic disease (secondary). In most cases of the latter, the systemic disease is an ANCA-associated vasculitis such as Wegener granulomatosis, microscopic polyangiitis, or Churg-Strauss syndrome.
Pathophysiology
In the pathophysiology of rapidly progressive glomerulonephritis the antineutrophil cytoplasmic antibodies (ANCA) interact with antigens in cytoplasm of neutrophils. It is thought that ANCA causes an early degranulation giving way to release of lytic enzymes at site of injury. ANCA are linked to the pathogenesis of glomerulonephritis, antineutrophil cytoplasmic antibodies specificity is determined via (ELISA), with pANCA(antibody) directed against MPO
In the pathophysiology of rapidly progressive glomerulonephritis the antineutrophil cytoplasmic antibodies (ANCA) interact with antigens in cytoplasm of neutrophils. It is thought that ANCA causes an early degranulation giving way to release of lytic enzymes at site of injury. ANCA are linked to the pathogenesis of glomerulonephritis, antineutrophil cytoplasmic antibodies specificity is determined via (ELISA), with pANCA(antibody) directed against MPO
Diagnosis
Serum analysis often aids in the diagnosis of a specific underlying disease. The presence of anti-Glomerular basement membrane (GBM) antibodies suggests type I RPGN; antinuclear antibodies (ANA) may support a diagnosis of systemic lupus erythematosus and type II RPGN; and type III and idiopathic RPGN are frequently associated with anti-neutrophil cytoplasmic antibodies (ANCA)-positive serum.
Serum analysis often aids in the diagnosis of a specific underlying disease. The presence of anti-Glomerular basement membrane (GBM) antibodies suggests type I RPGN; antinuclear antibodies (ANA) may support a diagnosis of systemic lupus erythematosus and type II RPGN; and type III and idiopathic RPGN are frequently associated with anti-neutrophil cytoplasmic antibodies (ANCA)-positive serum.
Impaired renal functions in an individual with 3 months or less of the condition is an indication of RPGN. An ultrasonographic examination of the abdomen should also be done. Upon urine examination, urinary sediment (proteinuria) can indicate proliferative glomerulonephritis, many cases of rapidly progressive glomerulonephritis need a renal biopsy to make a diagnosis.
Treatment
Therapy for rapidly progressive glomerulonephritis is done via corticosteroids and cyclophosphamide. The predictor of kidney survival is serum creatinine value. The substitution of azathioprine for cyclophosphamide after 90 day initial period is another option.Plasmapheresis can be used for patients who present with severe renal failure.Or with traditional chinese medicine.
Therapy for rapidly progressive glomerulonephritis is done via corticosteroids and cyclophosphamide. The predictor of kidney survival is serum creatinine value. The substitution of azathioprine for cyclophosphamide after 90 day initial period is another option.Plasmapheresis can be used for patients who present with severe renal failure.Or with traditional chinese medicine.
2015年11月5日星期四
2015年11月3日星期二
The color in Urine
Normal urine
Normal urine presents light yellow and bright color without sediments and turbidity. Urine color is affected by diverse factors, including water intake, temperature changes, food, and medicine. With high water intake, urine is colorless like plain boiled water. With low water intake and lots of sweat, urine appears yellow like beer. The conditions are normal.
Abnormal urine
Red color urine
Red color urine refers to hematuria, which means excessive red blood cell in urine. Hematuria is usually caused by nephropathy, stone, prostatitis, and bladder tumor. Once hematuria accompanies with severe pain in lower back, there appears stone, including renal stone and ureteral calculus.
Urine presenting soy color
When urine presents soy color, it indicates that lots of erythrocytes have been damaged. This situation is caused by acute nephritis, acute icteric hepatitis, and hemolytic jaundice.
Urine in white color
When there appears white color urine like milk, sometimes with white clot or blood in it, the symptoms refers to chyle in urine. The symptom is caused by filariasis or renal lymphatic blocking.
Yellow urine
Yellow urine may be caused by some medicines, such as berberine and vitamin B. If urine presents yellow for half a month without any medicine intake, people need be cautious for that. Yellow urine often indicates liver diseases, including hepatitis, gall stone, biliary tract blocking and obstructive jaundice.
There is no need to frighten when urine changes colors. It may be caused by food or some medicine, which will return to normal color in a few days. However, if urine presenting abnormal color for a long time, it is better to visit a doctor.
If you have any question, you can Email me by annadoctor.kidney@gmail.com
Normal urine presents light yellow and bright color without sediments and turbidity. Urine color is affected by diverse factors, including water intake, temperature changes, food, and medicine. With high water intake, urine is colorless like plain boiled water. With low water intake and lots of sweat, urine appears yellow like beer. The conditions are normal.
Abnormal urine
Red color urine
Red color urine refers to hematuria, which means excessive red blood cell in urine. Hematuria is usually caused by nephropathy, stone, prostatitis, and bladder tumor. Once hematuria accompanies with severe pain in lower back, there appears stone, including renal stone and ureteral calculus.
Urine presenting soy color
When urine presents soy color, it indicates that lots of erythrocytes have been damaged. This situation is caused by acute nephritis, acute icteric hepatitis, and hemolytic jaundice.
Urine in white color
When there appears white color urine like milk, sometimes with white clot or blood in it, the symptoms refers to chyle in urine. The symptom is caused by filariasis or renal lymphatic blocking.
Yellow urine
Yellow urine may be caused by some medicines, such as berberine and vitamin B. If urine presents yellow for half a month without any medicine intake, people need be cautious for that. Yellow urine often indicates liver diseases, including hepatitis, gall stone, biliary tract blocking and obstructive jaundice.
There is no need to frighten when urine changes colors. It may be caused by food or some medicine, which will return to normal color in a few days. However, if urine presenting abnormal color for a long time, it is better to visit a doctor.
If you have any question, you can Email me by annadoctor.kidney@gmail.com
订阅：
博文 (Atom)