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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abuse of analgesics (AA) is a well known cause of chronic interstitial nephritis. Recently a noxious effect of AA on the pancreas has been suggested based upon case observations, and first evidence for association of AA with chronic pancreatitis was presented. In the present prospective clinical study 95 patients with chronic renal insufficiency, in 53 of them associated with AA, were investigated for evidence of chronic pancreatitis (e.g. history of pancreatitis, pancreatic calcifications, diabetes and exocrine function). The patients were divided into two groups: group A consisted of 53 patients with chronic nephropathy associated with AA, and control group B consisted of 42 patients with chronic nephropathy of other etiology. Pancreatic calcifications were observed in 5 cases of group A (10%), but in none of the patients of group B. Exocrine insufficiency was found in 2 of the 5 cases with pancreatic calcifications. Only one of the 5 patients had a history of pancreatitis in association with exocrine and endocrine insufficiency. Thus pancreatic calcifications, which are virtually pathognomonic for chronic pancreatitis, were found exclusively in the group with chronic nephropathy due to analgesic abuse. Chronic pancreatitis in this group of patients is likely to be overlooked because of the lack of clinical and laboratory evidence. The present data support our previous observations that AA may be an etiological factor in chronic calcifying pancreatitis. This first evidence for a drug-induced form of chronic pancreatitis is presented.
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PMID:[Chronic pancreatitis as a possible result of analgesic abuse]. 358 21

To evaluate the role of glomerular hyperfiltration in the development and progression of diabetic nephropathy, we performed clearance and histopathologic studies in 24 rats with streptozocin-induced diabetes after 3 months of diets with different protein compositions. Calcium phosphate was added to an 8% protein diet in group I (nine rats), and calcium carbonate to a 24% protein diet in group II (nine rats) to equalize calcium and phosphate contents in these diets. Group I and II rats also received small doses of insulin to reduce the excessive hyperglycemia induced by the high sucrose content of the diets. In group III, six rats given an 8% protein diet, no calcium, phosphate, or insulin was added. In groups I and III, low dietary protein significantly reduced glomerular filtration rate and renal plasma flow per gram of kidney weight as compared with rates observed in group II rats with a higher protein intake. Features of diabetic glomerulopathy including mesangial hypercellularity and mesangial matrix expansion were also significantly milder in the groups with a low protein diet. On the other hand, medullary calcification and interstitial changes were most prominent in group I, given calcium phosphate supplement; the increase in the kidney weight was greater in groups I and II, which received insulin, than in group III, which did not. It was concluded that low protein diet significantly ameliorates diabetic glomerulopathy but that supplementation with inorganic phosphate in an amount equal to organic phosphate contained in the higher protein diet causes medullary calcification and interstitial nephritis. Also, administration of suboptimal doses of insulin in diabetic animals greatly enhances renal growth, more than that induced by diabetes alone.
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PMID:Effects of low-protein diet on experimental diabetic nephropathy in the rat. 390 11

Alloxan is known to induce diabetic renal changes as well as causing nephrotoxic alterations. However, no ultrastructural study has been performed to differentiate diabetic verses toxic affects of alloxan to the tubule and/or glomerulus. Therefore the present study used the "protected" kidney model to prevent one kidney from being exposed to the alloxan while allowing the other to receive the drug immediately. In all experimental animals the right renal hilum was gently occluded for 5 minutes and then released. This was performed prior to the injection of alloxan. Subsequently, the left renal hilum was occluded at the time of, and for 5 minutes after, alloxan administration (40 mg/kg i.v.). The experimental rats were divided into three groups: untreated diabetics, diabetics treated with protamine-zinc-insulin, and alloxan-treated rats that failed to become diabetic. Three groups of controls were included: one group received an equal volume of saline diluent as the experimental rats but no clamping of either renal hilum; another group received the saline and had the left renal hilum occluded for 5 minutes; and a third group had both the right and left renal hila occluded. All animals were followed and sacrificed after 9 weeks. Endogenous creatinine clearance did not change among groups. Alloxan-treated nondiabetic rats displayed marked interstitial nephritis in unprotected kidneys, while protected kidneys were normal. The diabetic state resulted in mesangial proliferation and focal glomerular basement membrane thickening as well as glomerular capillary endothelial abnormalities and visceral epithelial foot-process fusion. The endothelial changes consisted of focal areas showing a reduction in the size of endothelial fenestrae. All glomerular changes were ameliorated by insulin treatment. We conclude: 1) alloxan per se is distinctly nephrotoxic; and 2) the glomerular endothelium and epithelium are involved early in the course of experimental diabetes.
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PMID:The effect of alloxan, and alloxan-induced diabetes on the kidney. 671 36

This study was carried out to determine the prevalence of hepatitis C virus (HCV) antibodies and the epidemiologic factors associated with HCV infection in patients with chronic renal failure before the onset of ESRD. Sex, age, type of renal disease, level of renal function, and history of blood transfusions and invasive procedures were analyzed in 226 patients with renal disease, compared with a population of 1,244 normal subjects and 124 patients with impaired immunity (patients having autoimmune diseases and receiving chemotherapy treatment). Eighteen seropositive patients with renal disease (prevalence, 7.9%) were found, which was significantly higher than the prevalence in the normal population (1.03% in blood donors, 0.98% in pregnant women; P < 0.001, chi 2). There was no significant association of sex, number of blood transfusions, or history of invasive procedures with the presence of HCV antibodies. The prevalence of HCV antibodies was higher (16.6%) in patients with glomerulonephritis compared with patients diagnosed with interstitial nephritis, pyelonephritis, nephrosclerosis, diabetes mellitus, polycystic kidney, and miscellaneous renal diseases (P < 0.01, chi 2). There was a higher prevalence of HCV antibodies in patients with creatinine clearance lower than 30 mL/min (13%) compared with patients with creatinine clearance higher than 30 mL/min (2.7%) (P < 0.01, chi 2). These data suggest that HCV infection may be associated with the pathogenesis of glomerulonephritis. Alternatively, glomerulonephritis or severe renal insufficiency may increase the likelihood of HCV infection.
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PMID:Epidemiology of hepatitis C virus infection in patients with renal disease. 752 63

Analgesic nephropathy has long been considered a potentially preventable cause of renal disease. Early reports were described in patients who consumed analgesics containing phenacetin. In recent data, the removal of phenacetin from analgesic preparations resulted in a reduction in analgesic-induced end stage renal disease in Europe and Australia. However, a reduction in the incidence of analgesic nephropathy has not occurred uniformly, suggesting that phenacetin is not the sole cause. Current data raise concerns regarding adverse renal effects of acetaminophen and nonsteroidal antiinflammatory drugs. Aspirin taken alone may be of least concern. The diagnosis of analgesic nephropathy is suggested in subjects with chronic renal failure, a history of daily consumption of analgesic preparations, small bumpy kidneys, and renal papillary necrosis or chronic interstitial nephritis. However, the spectrum of disease may be changing, because these agents also may increase the risk of cardiovascular disease and chronic renal disease due to nephrosclerosis, glomerulonephritis, and diabetes mellitus. Potential pathogenetic mechanisms in analgesic nephropathy include direct cellular injury induced by analgesics, prostaglandin inhibition with reduction or redistribution of renal blood flow, and interesting new concepts regarding the role of caffeine in increasing oxygen demand and reducing oxygen supply in the medulla. The primary goal of therapy is discontinuation of analgesic consumption. Because of the association between analgesic intake and uroepithelial tumors, surveillance of patients for neoplasm is suggested.
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PMID:Case report: analgesic nephropathy: a soda and a powder. 757 21

We report the case of a white woman with insulin-dependent diabetes for 12 years who had rapid deterioration in renal function over a 7-month period. A renal biopsy showed widespread deposition of a polarizing crystalline material consistent with calcium oxalate. Fat malabsorption due to diabetic diarrhea was first documented 5 years earlier when renal function was normal. Chronic malabsorption can lead to chronic interstitial nephritis secondary to oxalate deposition, but rarely leads to acute deterioration in renal function. This entity should be considered in individuals with steatorrhea and no other cause for their renal failure.
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PMID:Rapid renal deterioration secondary to oxalate in a patient with diabetic gastroenteropathy. 761 Dec 71

This 1993 report of the Lombardy Regional Dialysis and Transplant Registry refers to all the data collected between January 1, 1983, and December, 31, 1992, by means of individual patient questionnaires sent to all of Lombardy's 44 renal units (100% replies). The number of patients recorded by the Registry as being alive progressively increased; by the end of 1992, the number was 6,014 (655 patients per million population): 4,770 patients were on dialysis treatment (515 patients per million population, 79.3%) and 1,244 patients (140 patients per million population, 20.7%) had received a kidney graft. The acceptance rate for dialysis increased from 64 per million population in 1983 to 102 per million population in 1992; the increase in the transplant rate was much lower (from 18.7 to 21.3 per million population). The percentage of primary nephropathies in the new patients accepted for dialysis treatment were 22.0% glomerulonephritis, 13.8% interstitial nephritis, 15.2% vascular diseases, 10.1% cystic kidney, and 10.6% diabetes. The use of acetate hemodialysis declined over the 10-year period from 72.4% to 17.5%; that of bicarbonate hemodialysis increased from 8.8% to 50.1% and that of hemodiafiltration increased from 0.2% to 11.1%. The prevalence of hospital hemodialysis was stable, ranging from 55.4% to 52.2%; home hemodialysis decreased from 15.7% to 5.3%, continuous ambulatory peritoneal dialysis increased from 13.3% to 19.6%, and limited care increased from 13.7% to 22.4%. The crude death rate increased from 7.5% in 1983 to 10.5% in 1992. The survival rate (Kaplan-Meier) of all patients on dialysis was 78.8% at 2 years, 62.2% at 4 years, and 40% at 8 years; for transplanted patients, the survival and graft survival rate at 2 years was, respectively, 95% and 86%. The relative death risk of the patients on peritoneal dialysis with respect to those on hemodialysis was 1.419, as estimated by the Cox proportional hazard regression model. The main causes of deaths of patients on dialysis treatment during the year 1992 were cardiovascular diseases (47.0%) and cachexia (19.5%); in transplanted patients, they were cardiovascular diseases (36.6%) and infections (34%). Registries are not only important for planning health care but are also very useful instruments for clinical research.
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PMID:1983 to 1992: report on regular dialysis and transplantation in Lombardy. 781 May 25

There is in the Western World a progressive ageing of the population, and consequently haemodialysis patients are also getting older. Some ethical questions have been raised as a consequence of the economic issues related to the scarcity of available resources. In this paper we review our experience in the treatment of very old chronic haemodialysis patients. Fifty patients (7.2% of our haemodialysis patients) aged over 80 years at the beginning of dialysis were included (f = 25, m = 26, age = 82.6 +/- 0.3 years). In 42% of the patients the aetiology of renal disease was unknown. In the remainder, the aetiology was: interstitial nephritis 26%, hypertensive nephrosclerosis 14%, chronic glomerulonephritis 8%, diabetes 8% and polycystic disease 2%. There was a great comorbidity: intradialytic hypotension 82%, cardiac disease 74%, gastrointestinal disease 32%, cerebrovascular disease 26%. Vascular access related problems were the main reason for hospitalization. The major cause of death was vascular (cardiac and cerebral disease). Actuarial survival was 89%, 78%, 56% and 48% at 6, 12, 24 and 36 months, respectively. We think that haemodialysis is the best available choice for treating very old chronic renal failure patients. However further studies are needed to improve the quality of life of these patients.
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PMID:Chronic haemodialysis for very old patients. 782 79

Reduced renal length is widely used to diagnose chronicity in patients with renal impairment. A length of 9 cm or less measured ultrasonographically is considered to indicate irreversible disease. However, some patients with normal renal length have thin parenchyma. The aim of this study was to determine the relationship between ultrasonographically measured parenchymal thickness and renal length and to correlate parenchymal thickness with the histology obtained at renal biopsy. Sixty-four patients, aged 16-74 years, who had had a renal biopsy were evaluated retrospectively. Histology was considered in five categories: I, interstitial nephritis (n = 13); II, glomerulonephritis (28); III, diabetes mellitus/metabolic/other (8); IV, chronic renal disease (CRD) (11); V, hypertension/vascular disease (4). There was a good linear correlation between renal length and renal parenchymal thickness (r = 0.64, P < 0.001). Both were reduced most in patients with CRD. Sixty-four per cent of patients with CRD had renal parenchymal thickness 1.5 cm or less, compared to 38% in group I, 25% in groups II and V, and 7% in group II. Although 11/37 (30%) of patients whose serum creatinine had increased 3 months post-biopsy had parenchymal thickness 1.5 cm or less, so did 6/27 (23%) whose creatinine decreased. Like renal length, parenchymal thickness gives an indication of the chronicity of renal failure. However, some patients with parenchymal thickness 1.5 cm or less still have potential for improvement. This measurement alone should not be used to obviate renal biopsy.
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PMID:What is the value of measuring renal parenchymal thickness before renal biopsy? 829 31

The incidence and risk factors of posttransplant diabetes mellitus were evaluated in 1325 consecutive renal transplant recipients. Thirty-three (2.5%) patients developed diabetes mellitus requiring insulin therapy. Onset occurred a mean of 5.7 +/- 1.5 months following transplantation. The patients were compared with 33 paired-control kidney recipients. The patients were significantly older than the controls (46.8 +/- 1.9 vs. 40.6 +/- 2.1 years) (P<0.05), and chronic renal failure was more often related to interstitial nephritis (P<0.05). A family history of diabetes mellitus, the body mass index, ethnic origin, HLA phenotype, and the total doses of steroids and cyclosporine were similar in the two groups. The number of patients with at least one rejection episode was significantly higher among the diabetic patients (21 versus 9) but the number of episodes was similar. Diabetes occurred a mean of 1.1 +/- 0.3 months following rejection treatment. Intravenous pulsed prednisolone was always used for anti-rejection therapy. Insulin was withdrawn in 16 cases after a mean of 4 +/- 1 months, independently of steroid dosage reductions. Actuarial patient and graft survival rates were not significantly different, although 6-year outcome tended to be better in the controls (86% versus 93% for patient survival and 67% versus 93% for graft survival). This study suggests that pulsed steroid therapy might be the critical factor in the onset of posttransplant diabetes and that the risk is increased in older patients with chronic interstitial nephrititis.
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PMID:Diabetes mellitus after renal transplantation: characteristics, outcome, and risk factors. 863 74


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