Decreased urine osmolality

Introduction Urine osmotic pressure, also known as urinary permeation, is the number of particles that reflect solute molecules and ions per unit volume of urine. The decrease in osmolality reflects the decrease in the concentration of the distal tubules, as seen in chronic pyelonephritis, chronic interstitial lesions caused by various causes, and chronic renal failure.

Cause

(1) Causes of the disease

Chronic pyelonephritis is common in women. Some patients have had acute urinary tract infections during childhood. After treatment, the symptoms disappear, but there are still "asymptomatic bacteriuria", which gradually develops into chronic pyelonephritis in adults. Some acute pyelonephritis is cured after infection by transurethral instruments. Poor urine flow (such as posterior urethral valve, bladder diverticulum, urinary tract stones and neurogenic bladder), vesicoureteral reflux is also the main cause of repeated urinary tract infection, renal scar formation, renal damage. Urinary tract infections of Gram-negative bacteria can cause systemic and local reactions. In patients with repeated infections, antibodies are increased. Most of these antibodies are IgG and IgA. IgG antibodies may form antigen-antibody complexes and fix complements, resulting in Kidney damage.

(two) pathogenesis

If susceptibility factors such as urinary tract obstruction, malformation and low body immune function persist, antibacterial therapy fails to completely control the inflammation or small abscess of the renal pelvis formed by acute pyelonephritis, leaving small scars and causing intrarenal obstruction. , causing repeated attacks and chronic delays. Some people think that the onset of chronic pyelonephritis may involve autoimmunity. Some patients found pathogenic bacteria in the urine culture of acute pyelonephritis, but in the later chronic process, there was no pathogenic bacteria in the urine culture, and the disease gradually entered chronic pyelonephritis. It is speculated that after kidney infection, the body produces antibodies against Escherichia coli, and kidney tissue has common antigenicity with these bacteria. After the pathogen disappears, the antibody continues to immunoreact with the kidney tissue antigen, causing kidney damage. A tubular antigen (Tamm-Horsfall protein, called THP) has been found to share antigenicity with Escherichia coli, and antibodies against Escherichia coli can simultaneously resist THP in renal tubular epithelial cells, which may be associated with kidney. Interstitial chronic inflammation is associated.

Modern studies have found that in any chronic kidney disease, once the inflammatory cell infiltration of the renal interstitial occurs, it is possible to cause renal tissue damage through the release of cytokines. The occurrence and development of chronic pyelonephritis may also be related to this.

The presence of L-type bacteria makes the treatment of pyelonephritis more difficult. These bacteria were first discovered by Lister, so the L-type bacteria were named. The formation is due to the rupture of the membrane of the pathogenic bacteria in the treatment of antibacterial drugs or by the action of antibodies, complements, lysozyme, only the original pulp, hidden in the hyperosmolar area of the renal medulla to survive, general antibacterial drugs Can't kill it completely. After the living environment improved, the L-type bacteria returned to their original shape, continued to grow and reproduce, and re-ignited the pyelonephritis, causing the disease to be delayed and difficult to treat. According to the investigation of chronic pyelonephritis with negative urine culture, about 20% of L-type bacteria can be found.

an examination

Related inspection

Urine routine renal function test

Laboratory inspection

1. Urine routine: may have intermittent pyuria or hematuria. Acute manifestations are the same as acute pyelonephritis.

2. Urine cell count: In recent years, the application of 1h urinary cell counting method, the criterion is: white blood cells > 300,000 / h is positive.

3. Urinary bacteriological examination: true bacterial urine can occur intermittently. In acute attacks, as with acute pyelonephritis, urine culture is mostly positive.

4. Blood routine: red blood cell count and hemoglobin can be slightly reduced. The white blood cell count and the proportion of neutrophils can be increased in acute attacks.

5. Renal function test: continuous renal damage can occur:

1 renal dysfunction, such as increased nocturia, morning urine osmotic pressure decreased.

2 acidification decreased, such as morning urine pH increased, urine HCO3- increased, urine NH4 decreased.

3 glomerular filtration function decreased, such as decreased endogenous creatinine clearance, blood urea nitrogen, creatinine and so on.

Film degree exam

1. X-ray examination: KUB plain film can show that one or both kidneys are smaller than normal. IVU can be seen in the size of the two kidneys, the shape is uneven, the renal pelvis and renal pelvis can be deformed, there is expansion and accumulation of water, the renal parenchyma becomes thin, there is a focal, rough cortical scar, accompanied by dullness of adjacent renal pelvis or Drumstick deformation. Sometimes the development is poor and the ureter is dilated. Some patients with urinary urinary tract have vesicoureteral reflux. In addition, there may be susceptibility factors such as poor urine flow, urinary tract obstruction such as stones, tumors or congenital malformations.

2. Radionuclide scanning: The patient's renal dysfunction can be determined, showing that the kidney is small, and the dynamic scan can also detect vesicoureteral reflux.

Cystoscopy may reveal inflammatory changes in the ureteral orifice of the affected side, ureteral intubation is blocked, and intravenous injection of rouge confirms impaired renal function.

3. Renal biopsy: light microscopy shows tubular atrophy and scar formation, interstitial lymphocytes, mononuclear cells infiltration, neutrophil infiltration in acute attacks, glomeruli can be normal or mild around the ball Fibrosis, if there is long-term high blood pressure, it can be seen that the glomerular capillary wall is hardened and the collagen in the glomerular capsule is deposited.

Differential diagnosis

Reduced urine specific gravity: Urine specific gravity measurement is used to estimate the concentrating function of the kidney, but the accuracy is poor and there are many factors affected. The measured values are for reference only. The decrease in urine specific gravity is seen in diabetes insipidus and chronic nephritis. The urine specific gravity is low, mostly below 1.020, and is often fixed at 1.010 in the late stage of the disease. Urinary protein traces ~+++. There are often red blood cells and casts in the urine (granular tube type, transparent tube type). There is obvious hematuria or gross hematuria during the acute attack.

Increased urine specific gravity: Urine specific gravity measurement is used to estimate the concentrating function of the kidney, but the accuracy is poor and the affected factors are many. The measured values are for reference only. Increased urine specific gravity is seen in dehydration, diabetes, acute nephritis and so on. The proteinuria is light and heavy (1~3g/d). There are microscopic hematuria. The red blood cells are pleomorphic and diverse. Sometimes, red blood cell casts, granular casts and renal tubular epithelial cells can be seen. Urinary fibrin degradation products (FDP) can be positive. Blood urea nitrogen and creatinine may increase transiently, serum total complement (CH50) and C3 decrease, return to normal within more than 8 weeks, and serum anti-streptolysin "O" titer may increase.

Increased urinary biliary: urinary biliary is derived from the binding of bilirubin. In combination with bilirubin in the lower part of the small intestine and in the colon, it is decoupled by the action of intestinal bacteria. After several stages of reduction, bilirubin becomes urinary biliary and then excreted with feces. A part of urinary biliary is absorbed into the portal vein from the intestine, most of which is taken up by the liver cells and then discharged into the intestinal fluid (intestinal hepatic circulation), and part of it enters the systemic circulation from the portal vein and is excreted from the urine through the kidney. A variety of factors can cause an increase in urinary biliary.

Increased urinary amylase: When pancreatitis and other diseases occur, pancreatic amylase enters the bloodstream and is excreted from the urine due to inflammation and other diseases in the pancreatic tissue, causing the patient's blood amylase to rise and amylase to be detected in the urine. Amylase assay, which is one of the important objective indicators for the diagnosis of acute pancreatitis, but not a specific diagnostic method. In the early stage of the disease, when there is embolism of the pancreatic blood vessels and some hemorrhagic necrotizing pancreatitis, it may not increase due to severe destruction of pancreatic tissue. Amylase may also increase in the case of shock, acute renal failure, pneumonia, mumps, perforation of ulcer disease, and intestinal and biliary infections. Therefore, when there is an increase in amylase, it is necessary to combine the history, symptoms and signs to rule out the increase of amylase caused by non-pancreatic diseases, in order to diagnose acute pancreatitis.

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