Hematuria With Increased Creatinine, 5 Steps To Clarify The Diagnosis

1 Is it nephrology hematuria?

In young female patients, the main clinical manifestation is the solution of red urine. Because the urine routine was not perfected before admission, it is called red urine. The possibility of false hematuria should be excluded, and some drugs (rifampicin, gentamicin, etc. ) and the influence of food, and a perfect urine routine indicate that there are red blood cells in the urine, and it is considered true hematuria.

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Because the patient is a young woman, we have ruled out the possibility of hematuria caused by menstruation by asking about her menstrual history. If the patient is not sure whether he is in the menstrual period, we can even perform a bladder puncture to identify the source of hematuria; at this time, we will first rule out the cause of systemic coagulation dysfunction. Cause hematuria, and then perfected the urine three-cup test to distinguish between medical-derived hematuria and surgical-derived hematuria.

Combined with the results of the urine three-cup test, it can be considered painless hematuria in the whole process (the results of the three urine routine tests are roughly the same), combined with the patient's urine routine, the number of red blood cells is 1001.8/μl, and the morphology of red blood cells is non-uniform, so it is judged to be the glomerular origin. Hematuria. Because the red blood cells are damaged by intravascular pressure through the broken basement membrane, and the damaged red blood cells are subjected to osmotic pressure and acid-base action through each segment of the renal tubule, so they appear as deformed red blood cells, the patient's urine routine indicates hematuria accompanied by proteinuria. , and there are manifestations of renal tubular damage such as decreased urine osmotic pressure, decreased urine specific gravity, and epithelial cell casts, which are considered to be hematuria caused by renal disease.

2 Which clinical syndrome is this?

The patient has no history of chronic renal failure, high-risk factors such as diabetes and hypertension, and no obvious abnormality in renal function, electrolytes, blood routine, urine routine, urinary color Doppler ultrasound, no proteinuria or edema, and low back pain. , increased nocturia, and other manifestations. After the patient was admitted to the hospital, the color Doppler ultrasound showed the size of both kidneys: the size of the right kidney was about 12.4x6.7x7.3cm, the thickness of the parenchyma was about 1.7cm, and the size of the left kidney was about 12.4x6.7x6.8cm, and the thickness of the parenchyma was about 2.1 cm. cm), the patient was of medium stature, the kidney size was average, and there were no chronic manifestations such as unclear cortico-medulla demarcation and cortical thinning, so it was excluded;

The main clinical manifestation of the patient is the solution of hematuria, and the auxiliary examination of tuberculosis does not contain massive proteinuria, hypoalbuminemia, edema and hyperlipidemia, and other manifestations of nephrotic syndrome, so it is excluded; The patient was a young female with acute onset, history of cold at onset, hematuria and renal insufficiency, no history of edema, oliguria, anuria, electrolyte disturbance, and severe acid-base balance disturbance. The patient took more medicine before admission. It is not ruled out that it is caused by drugs. At present, the possibility of acute nephritis and rapidly progressive glomerulonephritis is considered in renal insufficiency;

3 What disease is this?

The patient is young and female, with acute onset, hematuria, and renal insufficiency. The most likely diseases are acute nephritis and IgA nephropathy, both of which are commonly seen after strep bacterial infection. The former has a longer incubation period, usually 1- After 3 weeks (onset in about 10 days on average), serum C3 and total complement decreased at the beginning of the disease, and returned to normal within 8 weeks. The latter has a short incubation period, and gross hematuria may appear within hours to days after infection. The disease often recurs. In some patients, serum IgA is elevated, and serum C3 is normal.

Considering the relevant clinical characteristics of the patients: IgA nephropathy is highly likely. Because the etiology of the patient is unknown and combined with renal insufficiency, a clear disease is a premise for formulating a treatment plan. In addition, histopathological examination of renal biopsy is a necessary method for the diagnosis of IgA nephropathy. The creatinine was higher on admission, and hemodialysis was given several times to reduce the creatinine. After reducing the risk of puncture, a renal puncture biopsy was performed.

The pathological report of kidney biopsy indicated: 1. Conform to mild mesangial proliferative IgA nephropathy, Lee grade II; 2. Acute tubular-interstitial injury, so the disease was definite.

4 What is the cause?

It is necessary to distinguish primary kidney disease from secondary kidney disease. Primary kidney disease includes immune response-mediated nephritis, urinary tract infection, renal blood vessels, kidney tumors, and other diseases; secondary kidney disease can be secondary to other tumors, metabolic disorders, etc., autoimmune diseases and various drugs and poisons cause damage to the kidneys.

Combined with this medical record, it is most necessary to exclude renal diseases caused by allergic purpura and systemic lupus erythematosus. According to the patient, the patient has no discoid erythema, butterfly erythema, photosensitivity, oral ulcers, alopecia, and multi-system damage, and no immune-related indicators (ds-DNA, antiphospholipid antibody, anti-SM, anti-blood cell antibody, etc.) were abnormal, so they were excluded; the patient had no recent history of allergies, no skin purpura symmetrically distributed on both lower extremities, no abdominal pain, no joint swelling and pain, and other related symptoms, so be excluded. 

It was finally identified as primary IgA nephropathy with acute tubular-interstitial injury.

5 How to treat?

The pathological changes and distribution changes of IgA nephropathy in different medical records are complex and diverse, and its pathological classification standards have been under study, including the Lee classification in 1982, the Haas classification in 1997, and the Oxford classification in 2009-2017. 

Treatment-optimized supportive care includes blood pressure management, maximum tolerated doses of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, lifestyle modifications (sodium restriction, appropriate exercise, etc.), and avoidance of nephrotoxic drugs Wait.

Primary IgA nephropathy, Lee grade II, this pathological damage is relatively mild, and hormone therapy may not be required, but it is combined with acute tubular-interstitial injury. To prevent interstitial fibrosis, hydrochloride should be given immediately after the pathological results are reported. No injection 6of 0mg anti-inflammatory treatment, supplemented with aluminum magnesium carbonate chewable tablets to protect the stomach, calcium carbonate D3 tablets to prevent hormone-related osteoporosis.

After the relevant treatment, the hematuria disappeared and the creatinine was significantly lower than before, but the patient still needed to take prednisone acetate tablets for anti-inflammatory for a long time after discharge, and told the patient to adjust the dose under the guidance of a specialist physician, and do not stop the drug or take it by himself. Reduce the dose to avoid the recurrence of the disease.

for more information:ali.ma@wecistanche.com