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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute renal failure developed in a 3-year-old boy with acute pyelonephritis. Renal biopsy showed acute interstitial infiltration of neutrophils and macrophages. There were also glomerulitis and capillary tuft thrombosis. He required peritoneal dialysis, but subsequently recovered renal function. Prompt antimicrobial therapy is crucial to insure a favorable outcome. Pyelonephritis is an unusual cause of acute renal failure in infants and children.
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PMID:Acute renal failure due to pyelonephritis. 231 42

Nine fatal cases of systemic mucormycosis observed in association with renal failure are described. Four patients were hospitalized for chronic renal failure as a consequence of chronic glomerulonephritis, myeloma kidney, chronic pyelonephritis, and polycystic kidney disease, respectively; and five patients presented with acute renal failure. The underlying causes in three of these five patients were gentamycin nephrotoxicity, acute gastroenteritis, and allograft rejection, respectively, and in the remaining two, acute renal failure was the result of extensive renal vascular and parenchymal invasion by mucor hyphae. Tissue invasion with mucormycosis was documented during life in two patients and at autopsy in seven patients. The infection was disseminated in five patients, and isolated pulmonary and rhinocerebral involvement occurred in two patients each. Our observations have shown that patients with renal failure are prone to develop mucormycosis, which carries a grave prognosis if therapy is not instituted in time.
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PMID:Mucormycosis in patients with renal failure. 248 82

Renal complications were studied in 81 autopsied patients suffering from multiple myeloma (47 male, 34 female, mean age 66.3 years). Kidney samples were examined for the presence of Bence Jones cast nephropathy, light chain deposition disease, amyloidosis, nephrocalcinosis, chronic urate nephropathy, acute renal failure, renal vein thrombosis, acute and chronic pyelonephritis, and tumorous infiltration of the kidney tissue. Lesions were graded under the light microscope as minimal, mild, moderate or severe. This grading and the corresponding serum creatinine levels were used to distinguish four groups: 1. morphologically and functionally intact kidney (40 cases); 2. kidney involvement with good renal function (10 cases); 3. kidney involvement with moderate chronic renal insufficiency (16 cases); 4. kidney involvement with chronic uraemia (15 cases). In patients with an impaired renal function (groups 3 and 4), Bence Jones cast nephropathy occurred most frequently (27 cases, 33%); all other complications were seen much less frequently. Among the 81 patients, two cases of kappa light chain deposition disease and three cases of amyloidosis were found. Although the semiquantitative morphology and serum creatinine levels displayed a good correlation, there were cases with marked histological changes but only a moderate impairment in renal function, suggesting that the drawing of functional conclusions from morphological changes of the kidney requires caution.
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PMID:Renal complications in multiple myeloma. 248 64

One hundred adult Sudanese patients who presented to Soba University Hospital (SUH) with established chronic renal failure (CRF) were studied to determine the aetiology. Thirty-eight had chronic glomerulonephritis, 12 renal calculi, nine diabetic renal disease, seven chronic pyelonephritis, five sequelae of acute renal failure (ARF), four renal vascular disease, three polycystic disease of the kidneys, and two obstructive uropathy. In 20 patients the aetiology was not determined because of late presentation to hospital. The results were compared with those of the developed countries, which differ greatly from Sudan in climate, diet, race, culture and social habits. The main differences were in the prevalence of renal calculi which, although being the second commonest cause of CRF in the Sudan, were rare in European countries. Also, diabetes mellitus was a much commoner cause of CRF in Sudan than Europe. Other aetiological factors were similar.
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PMID:The aetiology of chronic renal failure in adult Sudanese patients. 260 79

A case of emphysematous pyelonephritis with septic shock was present in a 58-year-old diabetic woman. The spontaneous production of gas was present within the right renal pelvis in kidney-ureter-bladder X-ray. The patient's condition deteriorated rapidly after admission, became complicated with acute renal failure, disseminated intravascular coagulation and acute respiratory failure. Transurethral drainage of the pelvis using a 6 Fr. UPJ occlusion balloon catheter and endotracheal intubation with respiratory assistance were performed as a life-saving procedure. The optimal therapy with surgical or conservative approach for such a severe condition is discussed. The use of transurethral drainage of pelvis as a non-invasive treatment is suggested.
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PMID:[A case of emphysematous pyelonephritis with septic shock recovered by transurethral drainage of pelvis]. 267 63

24 patients with chronic renal failure due to chronic pyelonephritis were studied prospectively. In 18 of them (51%) the deterioration of the renal function was caused by obstruction, urinary infection, dehydration, etc. In 13 patients with chronic renal failure in exacerbation there were clinical data for activation of the pyelonephritis which was followed up dynamically. The ultrasound examination revealed enlarged kidneys with unclearly outlined renal structures. The changes were reversible and the pattern resembled that of acute renal failure. With the disappearance of the echographic data for interstitial renal edema an improvement of the renal function was established. The serum creatinine fell from 697.4 to 347.6 mumol/l (p less than 0.025) and plasma osmolality tell from 327.8 to 287 mOsm/l. No such changes were found in other II patients with chronic pyelonephritis and chronic renal failure without exacerbation.
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PMID:[Clinico-echographic parallels in patients with pyelonephritis and exacerbated chronic kidney failure]. 269 16

This paper reports the only 6 cases of ureteric obstruction apparently caused by the gravid uterus diagnosed at the Mercy Maternity Hospital in the past 17 years, during which time there were 82,836 confinements. In 3 of the 6 cases there was clear radiographic evidence that the level of obstruction was at the pelvic brim. The rapid resolution of the ureteric obstruction shortly after delivery strongly suggested that the gravid uterus was the cause of the obstruction. Cases 1-3 were the only patients of 793 with polyhydramnios who developed bilateral ureteric obstruction and acute renal failure. In Cases 4 and 5 there was unilateral ureteric obstruction and pyelonephritis; in Case 4 a ureteric catheter was inserted from below, and in Case 5 a ureteric stent was inserted via a nephrostomy tube. In Case 6 a percutaneous nephrostomy tube was inserted.
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PMID:Ureteric obstruction by the gravid uterus. 269 55

A sandwich ELISA assay has been formatted from two commercially available murine monoclonal antibodies, URO-4 and URO-4a, directed against a 120,000 dalton glycoprotein, the adenosine deaminase binding protein (ABP), found on the brush border of the renal proximal tubular epithelial cell. Untimed urine samples from 37 normal individuals and urinary ABP less than 0.1 AU; 37 patients with pure glomerular disease had ABP less than 0.4 AU (with 29, or 76% less than 0.2 AU); 10 patients with pre-renal azotaemia had ABP less than 0.6 (with 8, or 80% less than 0.3 AU). In contrast, 79 patients with post-ischaemic acute tubular necrosis had ABP greater than 0.6 AU. Acute renal failure due to myoglobinuria, contrast dye, and aminoglycoside toxicity were all associated with urinary ABP greater than 1.0 AU. In addition, all six patients with acute bacteraemic pyelonephritis had ABP greater than 0.7 AU, as opposed to ABP less than 0.2 AU in the urines of 12 women with acute cystitis. We conclude that this monoclonal antibody based urinary assay is a sensitive measure of renal proximal tubular injury, reliably distinguishes acute tubular from glomerular disease, and may be helpful in differentiating forms of urinary tract infection.
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PMID:Diagnosis of renal proximal tubular injury by urinary immunoassay for a proximal tubular antigen, the adenosine deaminase binding protein. 288 57

Acute renal failure is a most challenging clinical problem when it occurs in pregnancy. It requires an understanding of the normal physiology of the kidney in pregnancy and the natural history of different underlying renal diseases when pregnancy occurs. Because patients with chronic renal disease may present with worsening proteinuria, hypertension, and renal function, these disorders must be excluded from those conditions that cause acute deterioration of renal failure in otherwise normal women during pregnancy. As in all patients who develop acute renal failure, prerenal and obstructive causes must be excluded. Particularly important causes of prerenal azotemia in pregnancy include hyperemesis gravidarum and uterine hemorrhage, especially if it is unsuspected as in abruptio placentae. Infectious causes of acute renal failure in the pregnant woman include acute pyelonephritis and septic abortion. The clinical presentation of both these conditions should be apparent, and appropriate diagnosis and treatment can then be promptly instituted. Renal cortical necrosis is another cause of renal failure that occurs more frequently in pregnancy, and it must be differentiated from the many causes of acute tubular necrosis that may be associated with pregnancy. Those conditions that cause renal failure unique to pregnancy must always be considered when renal function deteriorates in the last trimester or the postpartum period. Severe preeclampsia, acute fatty liver of pregnancy, and idiopathic postpartum acute renal failure may all present similar complications, but the approach to each of these clinical disorders must be individualized. By understanding the causes of renal functional deterioration in pregnancy, a logical differential diagnosis can be established, allowing appropriate therapeutic decisions to preserve both maternal and fetal well-being.
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PMID:Acute renal failure in pregnancy. 305 11

The progression of renal failure was analyzed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosuppressive treatment. The reciprocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephropathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p less than 0.01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration. For those with linear progression of renal failure there was a significant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure. Calcium phosphate product correlated poorly with the rate of deterioration. We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure. Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephritis.
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PMID:Renal pathology and proteinuria determine progression in untreated mild/moderate chronic renal failure. 320 6


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