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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oliguric acute renal failure occurs in some adult patients with minimal change glomerulopathy. To look for clinical and pathologic factors that increase the risk for developing acute renal failure, 21 adults with minimal change glomerulopathy and a serum creatinine greater than 177 mumol/L (mean, 486 mumol/L; range, 194 to 1,344 mumol/L) (greater than 2.0 mg/dL [mean, 5.5 mg/dL; range, 2.2 to 15.2 mg/dL]) were compared with 50 adults with minimal change glomerulopathy and a serum creatinine less than 133 mumol/L (mean, 88 mumol/L; range, 53 to 124 mumol/L) (less than 1.5 mg/dL [mean, 1.0 mg/dL; range, 0.6 to 1.4 mg/dL]). Minimal change glomerulopathy patients with acute renal failure were older (59.5 v 40.3 years, P less than 0.001), and had higher systolic blood pressure (158 v 138 mm Hg, P = 0.001), more proteinuria (13.5 v 7.9 g/24 h, P = 0.01), and more arteriosclerosis in the renal biopsy specimen (1.7 + v 0.7 + on a scale of 0 to 4+, P = 0.005). Tubular epithelial simplification identical to that observed with ischemic acute renal failure (acute tubular necrosis) was observed in 71% of the patients with serum creatinine greater than 177 mumol/L (greater than 2.0 mg/dL) and 0% of those with less than 133 mumol/L (less than 1.5 mg/dL). All 18 patients with renal failure for whom follow-up data were available had recovery of function (mean creatinine, 539 +/- 301 mumol/L [6.1 +/- 3.4 mg/dL] at the time of biopsy and 106 +/- 27 mumol/L [1.2 +/- 0.3 mg/dL] at last follow-up), but sometimes only after weeks of dialysis support.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adult minimal change glomerulopathy with acute renal failure. 223 33

The association of HBV infection and glomerular damage was first reported by Combes et al in 1971, in a patient with nephrotic syndrome due to membranous glomerulopathy and chronic hepatitis B. Since, then, other glomerular diseases have been reported such as a) minimal changes nephropathy, b) IgA nephropathy, c) membranous-proliferative glomerulonephritis (MPGN), d) membranous, e) mesangial proliferative and f) lupus nephritis. All of them are associated with chronic hepatic disease and some of the following antigens: 1) HBsAg; 2) HBeAg; 3) HBcAg. These disorders are very frequent in Southeast Asia. Vertical transmission from mothers to fetuses may be important in maintaining the high carrier rate, and possibly plays a role in the development of glomerular damage. On the other hand, MPGN associated with HBsAg has rarely been reported and always with a favorable benign course. The present report describes interesting findings in a renal biopsy from a HBsAg and HBeAg carrier, who developed renal failure requiring hemodialysis. A 21 year old Korean man was admitted to the Hospital for nephrotic syndrome, microhematuria hypertension and renal failure. He had no previous history of blood transfusion, intravenous drug addiction, jaundice or liver disease. His father was HBsAg carrier with hepatic cirrhosis. An ultrasound examination showed normal renal size. Renal biopsy was performed and the patient received hemodialysis treatment. The specimen was processed for light microscopy, immunofluorescent studies and peroxidase-antiperoxidase technique. Frozen sections were studied by direct immunofluorescence for the identification of IgG, IgA, C1q, C3, fibrinogen and albumin. Paraffin sections stained by immunoperoxidase technique for HBsAg, using polyclonal monospecific rabbit anti-Human antisera (Dakopatts, Copenhagen).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Membranoproliferative glomerulonephritis with semilunar forms and massive deposits of IgA associated with HBsAg]. 229 14

A high prevalence of renal failure has been reported in bull terriers in Australia. The pattern of inheritance was analysed in a family of 33 bull terriers in which 10 dogs had renal disease manifested by proteinuria, ultrastructural abnormalities in the glomerular basement membrane, renal failure, or 'end stage' kidneys. The presence of at least one affected parent for each affected offspring, the approximately equal male/female ratio and the apparent absence of 'generation-skipping', strongly supported an autosomal dominant mode of inheritance, assuming a fully penetrant single major gene locus. Further evidence was not compatible with either an autosomal recessive or X-linked inheritance pattern. This contrasts with the X-linked inheritance shown in Alport's-type human hereditary nephritis and hereditary glomerulopathy in the samoyeds. Hereditary nephritis in the bull terrier should be a useful model for non-Alport's-type human hereditary nephritis, which is also reported to have an autosomal dominant inheritance pattern.
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PMID:Hereditary nephritis in the bull terrier: evidence for inheritance by an autosomal dominant gene. 235 1

We studied the clinical and pathological data for 334 patients age 65 or more who underwent renal biopsy for acute renal failure (ARF, n = 55), subacute renal failure (SRF, n = 72), chronic renal failure (CRF, n = 57), proteinuria (n = 137), and hematuria (n = 13). Tissue diagnoses were glomerulopathy (n = 252, 75.4%), acute tubular lesions (n = 18), interstitial nephritis (n = 23), vascular diseases (n = 36, including 14 with cholesterol emboli), and five miscellaneous diagnoses. Of the 55 patients with ARF, 23 had a glomerular lesion, 15 had acute tubular necrosis, and 8 had acute interstitial nephritis. Of 72 patients with SRF, 49 had a glomerulopathy, 12 had a vascular disorder, and six had acute interstitial nephritis. Hence, patients with ARF or SRF exhibited a high potential for reversible lesions. Only 11.3% of patients with CRF had potentially reversible causes. The most common causes of proteinuria were membranous glomerulopathy (34.3%), minimal change disease (14.6%), focal segmental sclerosis (11.7%), and amyloidosis (8.8%). Of the 25 patients with advanced nephrosclerosis, 24 had renal failure, 20 were hypertensive, and 13 had cholesterol emboli. Of 33 patients with diabetes mellitus, 66.7% were found to have lesions not related to diabetes. We conclude that renal biopsy is most useful in older patients with ARF or SRF because of potentially reversible renal disease. Old age alone is not a contraindication to performing a renal biopsy.
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PMID:Renal biopsy in patients 65 years of age or older. An analysis of the results of 334 biopsies. 235 29

A 61-year-old women presented with nephrotic syndrome and progressive renal failure associated with metastatic adenocarcinoma of the liver. Renal biopsy revealed marked widening of the basement membrane and nonamyloidotic fibrillary deposits composed chiefly of polyclonal IgG. This is the first reported case of Congo-red-negative fibrillary glomerulopathy in association with adenocarcinoma of the liver.
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PMID:Fibrillary glomerulonephritis in a patient with metastatic carcinoma of the liver. 238 87

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
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PMID:Acromegaly in 14 cats. 240 66

Samoyed hereditary glomerulopathy (SHG) is an X-linked dominant disease characterized by proteinuria and renal failure in affected male dogs. Electron microscopic examination of glomerular capillary basement membranes (GCBM) shows widespread multilaminar splitting of the lamina densa, identical to that in Alport's syndrome. Anionic sites in GCBM of three affected males and five unaffected dogs were labeled using polyethyleneimine to determine whether proteinuria was associated with an alteration in their number. No significant differences were noted in the number of anionic sites in the lamina rara externa, whereas small but statistically significant increases were seen in the number of sites in the lamina rara interna of affected males. In the lamina densa, affected males showed a striking increase in anionic sites, particularly in regions of GCBM which were split. Thus, although proteinuria in some glomerular diseases has been attributed to a reduction in anionic sites in GCBM, this was not so in SHG.
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PMID:Quantitation of anionic sites in glomerular capillary basement membranes of Samoyed dogs with hereditary glomerulopathy. 243 92

The pathogenesis of terminal renal failure is discussed. The following are distinguished: 1. Renal failure occurring against a background of decompensated benign nephrosclerosis, primary and secondary malignant nephrosclerosis, and stenosis of the renal artery. 2. Renal failure caused by loss of glomeruli. It is pointed out that in most glomerulopathies, including diabetic glomerulopathy and renal amyloidosis, terminal renal failure only develops when accompanying disease of the postglomerular vessels leading to interstitial fibrosis impairs the outflow of blood from the glomerulus to such an extent that no more urine is produced. 3. Renal failure in disease of the tubules themselves. It is emphasized that acute renal failure only becomes chronic when interstitial fibrosis develops from the interstitial edema occurring in the early stage of the disease. 4. Renal failure occurring in primary diseases of the renal cortical interstitium. The chronic sclerosing renal diseases arising from acute interstitial nephritis are dealt with, as also are reflux nephropathy, incomplete obstructive nephropathy, analgesic nephropathy, and chronic interstitial rejection reactions in transplanted kidneys.
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PMID:[The pathogenesis of chronic renal failure]. 248 15

Schistosomiasis mansoni has been well documented as one of the causes of infectious glomerulopathy, with mesangiocapillary glomerulonephritis being the most frequent lesion observed in this condition. Twenty-one patients with hepatosplenic schistosomiasis mansoni and biopsy-documented mesangiocapillary glomerulonephritis (MCGN) were studied and compared with 19 patients with the idiopathic form of MCGN. Nephrotic syndrome was the most frequent clinical presentation in both groups. At the time of diagnosis nine patients with hepatosplenomegaly (4 with associated arterial hypertension) and 12 (8 with arterial hypertension) among the patients with idiopathic MCGN had renal insufficiency. At the end of the follow-up period 16 patients with hepatosplenic schistosomiasis and MCGN (75.2 months) and 15 with the idiopathic form (52.1 months) had renal failure. Also, when compared at 48 months of follow-up, no difference in renal function could be detected in both groups. No benefits related to anti-parasitic treatment in the schistosomiasis group and immunosuppression therapy in either group could be documented. The progression of the renal disease, as assessed by the reciprocal of serum creatinine versus time, and the survival curve, were not different between the two groups. It is concluded that MCGN in patients with the hepatosplenic form of schistosomiasis mansoni is a progressive disease not influenced by anti-parasitic or immunosuppressive therapy, and presents a clinical course similar to that of the idiopathic form.
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PMID:Schistosoma mansoni-induced mesangiocapillary glomerulonephritis: influence of therapy. 250 87

The pathogenesis of terminal renal failure is discussed. The following are distinguished: 1. Renal failure occurring against a background of decompensated benign nephrosclerosis, primary and secondary malignant nephrosclerosis, and stenosis of the renal artery. 2. Renal failure caused by loss of glomeruli. It is pointed out that in most glomerulopathies, including diabetic glomerulopathy and renal amyloidosis, terminal renal failure only develops when accompanying disease of the postglomerular vessels leading to interstitial fibrosis impairs the outflow of blood from the glomerulus to such an extent that no more urine is produced. 3. Renal failure in disease of the tubules themselves. It is emphasized that acute renal failure only becomes chronic when interstitial fibrosis develops from the interstitial edema occurring in the early stage of the disease. 4. Renal failure occurring in primary diseases of the renal cortical interstitium. The chronic sclerosing renal diseases arising from acute interstitial nephritis are dealt with, as also are reflux nephropathy, incomplete obstructive nephropathy, analgesic nephropathy, and chronic interstitial rejection reactions in transplanted kidneys.
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PMID:The pathogenesis of chronic renal failure. 269 36


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