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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus is a prevalent disorder, well controlled in many persons with prolongation of life. Several radiologic manifestations are sufficiently specific to suggest a diagnosis in the unidentified patient, but even more important is an awareness of the sometimes life-threatening complications of diabetes which can be diagnosed from uroradiologic studies. We review the following urinary tract manifestations and complications of diabetes: pyelonephritis, perinephric abscess, renal papillary necrosis, emphysematous pyelonephritis, emphysematous cystitis, fungus infections, calcification of the vas deferens, seminal vesicle, and intrarenal branches of the renal artery, neuropathic bladder, and renal failure.
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PMID:Uroradiology of diabetes mellitus. 97 1

The polyols, sorbitol and myo-inositol, seem to be involved in the development of diabetic complications of different organs. High concentrations of both polyols were found in kidney medulla in addition to trimethylamines. To investigate the influence of diabetes mellitus on the regulation of both polyols and glycerophosphorylcholine in kidney, these osmolytes were quantitated enzymatically along the corticopapillary axis in untreated, streptozotocin-diabetic and insulin-treated streptozotocin-diabetic rats. In control animals three individual osmolyte patterns were found: a steep gradient of sorbitol in the papilla, increasing amounts of glycerophosphorylcholine from the outer medulla to the papilla, and nearly equal amounts of myo-inositol in the renal medulla, decreasing towards the cortex. Diabetic rats exhibit an up to fourfold increase of inner medullary sorbitol, whereas myo-inositol was only elevated in the outer medulla. Glycerophosphorylcholine was lowered in the papillary tip and elevated in the outer medulla and cortex. Insulin treatment reduced sorbitol to a concentration between those of diabetic and control rats, caused a restoration of glycerophosphorylcholine in the papillary tip and outer medulla to control values, and increased cortical myo-inositol. These data confirm previous in vitro data, which show that papillary sorbitol specifically increases in hyperglycaemic states, thereby counteracting the increased extracellular tonicity due to elevated tissue glucose concentrations. Imbalance of extra- vs intracellular osmolality during insulin treatment may be involved in the pathomechanism of renal papillary necrosis.
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PMID:Renal sorbitol, myo-inositol and glycerophosphorylcholine in streptozotocin-diabetic rats. 149 53

The pediatric nephrologist has traditionally not been involved in the care of the diabetic child since diabetic nephropathy presents in adulthood. Recent studies suggest that diabetic kidney disease develops silently during childhood. Measurement of urinary albumin excretion (UAE) allows earlier detection of patients at risk of nephropathy, often in adolescence. In addition to diabetic nephropathy, diabetic children are at risk of urinary tract infections, renal papillary necrosis, and various forms of glomerulonephritis. The role of the pediatric nephrologist in the care of the child with diabetes might include advising on the administration and interpretation of screening for UAE and the measurement and interpretation of glomerular filtration rate, and blood pressure. Children with evidence of renal dysfunction should be evaluated and treated by the pediatric nephrologist. Frequently, renal biopsy will be necessary in these patients. Future research may allow the detection of diabetic kidney disease earlier in childhood, further expanding the role of the pediatric nephrologist. In particular, early renal biopsy may eventually be used to select those patients at risk of diabetic nephropathy for specific treatment alterations.
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PMID:The role of the pediatric nephrologist in the care of children with diabetes mellitus. 186 94

Although diabetes mellitus is reported in 29% of patients with renal papillary necrosis (RPN), the frequency of RPN among patients with insulin-dependent diabetes mellitus (IDDM) has from autopsy studies been estimated to be only 4.4%. In vivo data on the prevalence of RPN in patients with IDDM have been lacking. We therefore studied the prevalence of RPN in 76 patients with long-standing IDDM and in 34 age-matched control subjects by intravenous urography. None of the control subjects showed radiographic signs of papillary necrosis. RPN was observed in 18 patients (23.7%); 15 were women (83.3%). Age and duration of diabetes was not different between patients with and without papillary necrosis, and there was no significant difference between the two groups regarding the prevalence of microangiopathic complications, i.e., proliferative retinopathy and diabetic nephropathy. Microscopic hematuria was three times more frequent in patients with than without RPN (44 vs. 16%; P less than .02). In addition, pyuria was reported in 40% of patients with papillary necrosis, and 61% of them gave a positive history of urinary tract infection compared to 16% (P less than 05) and 32% (P less than .02), respectively, in patients without papillary necrosis. It is concluded that RPN is a more frequent complication of long-standing IDDM than appreciated from autopsy studies, and being female and having a history of urinary tract infection are associated with an increased risk of RPN.
Diabetes Care 1989 Mar
PMID:Renal papillary necrosis in patients with IDDM. 270 11

Hematuria of unknown origin occurs in 30% of patients with diabetic nephropathy. In nondiabetic persons, hematuria may be caused by hypercalciuria with or without nephrolithiasis. Eight children with type I diabetes mellitus, hematuria, and hypercalciuria were observed in our clinic during a 1-year period. Two of these also had evidence of renal papillary necrosis. To assess the importance of hypercalciuria in the pathogenesis of hematuria in children with diabetes mellitus, we measured urinary calcium excretion in a large population of such patients. The calcium to creatinine ratio in the urine of diabetic children (0.21 +/- 0.01) was greater than that of nondiabetic children (0.12 +/- 0.01). A calcium to creatinine ratio of 0.28 was established as the upper limit of normal in our nondiabetic population, and 27% of the diabetic children were hypercalciuric on this basis. The diabetic children with hypercalciuria also had hyperphosphaturia and a urinary CaHPO4 X 2H2O molar ion product three times that found in the nondiabetic control population. These data suggest that many children with diabetes are at risk for renal damage due to hypercalciuria. Because hypercalciuria is more common in diabetic than nondiabetic children, it may play a previously unrecognized role in the renal disease associated with diabetes mellitus.
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PMID:Hematuria and hypercalciuria in children with diabetes mellitus. 357 34

Eighty-six cases of renal papillary necrosis (RPN) published in Japan over the years 1949-1980 were studied. While several hundreds cases of RPN were reported in certain European countries and the USA, only 5 cases were published in Japan up until 1960. However, the number of case reports has increased to 28 over the 5 year period of 1976-1980. The ratio of diabetics (62 cases) to nondiabetics (24 cases) is about 2.6:1 and is the same as that reported by Lauer in the USA. In diabetics, RPN was more frequently seen in females (3.4:1) and at more advanced age. Frequency of bilateral occurrence was high (47.5%). The prevalence of the association of glomerulosclerosis (75.0%) was higher than that reported by Silverman et al. in the USA (47.1%). The Incidence of the association of disturbances of consciousness (29.5%) was similar to that reported by Edmondson et al.. It was concluded that the number of cases of RPN with diabetes mellitus in Japan started to increase about 20 years later than in the USA, and that the frequency of the association between RPN and diabetic glomerulosclerosis in Japan seems to be higher than in the USA. Furthermore, it was noted that RPN was frequently associated with hyperosmolar nonketotic diabetic coma.
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PMID:Epidemiological studies on renal papillary necrosis with diabetes mellitus in Japan. 668 May 17

Aldose reductase (AR) has been purified from canine kidneys, and a monospecific antibody against the enzyme prepared. These antibodies were used in an immunohistochemical test to detect tissue sites of aldose reductase in the dog, a species known to develop diabetic lesions morphologically identical to those seen in diabetic patients. Using this method, the enzyme has been demonstrated in numerous cell types, including lens epithelium, aortic endothelium and smooth muscle, Schwann cells of peripheral nerves, and, in the kidney, interstitial cells and cells of Henle's loop and the collecting tubules. Many other cells and tissues, including capillaries throughout the body, lack immunoreactive aldose reductase. The distribution of the immunoreactive enzyme is compatible with a potential role of the enzyme in the aetiology of some complications of diabetes, namely cataract, neuropathy, macroangiopathy and renal papillary necrosis, but not the microvascular complications.
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PMID:Immunohistochemical distribution of aldose reductase. 681 8

The clinical and diagnostic features of renal papillary necrosis (RPN) of 27 patients were studied. Diabetes mellitus was the most frequent (56%) condition associated with RPN. Analgesic abuse, sickle hemoglobinopathy and urinary tract obstruction were present in 4 patients each; in 6 of these 12 patients these conditions were present as a coexistent disease with diabetes mellitus. There was evidence of an acute or chronic infection of the urinary tract in 18 patients, as a coexistent condition with another underlying disease that itself can cause RPN in 14 patients and as the only cause of RPN in another 4. Thus, the presence of more than one diagnostic condition which might be implicated in the causation of RPN was present in 15 patients or 55% of the cases in this series. When infection was excluded, six patients or 22% of the cases had two coexisting diseases, each of which has been implicated as a cause of RPN. This observation underlines the multifactorial nature of this entity and might explain why RPN is not encountered more frequently in each of the various primary diseases with which it has been associated. The average age of the patients at the time of diagnosis was 53 years for women and 56 years for men. Only six of the patients were younger than 40 years, and three of these had sickle hemoglobinopathy. The diagnosis of RPN was based on x-ray findings in eight patients, on the histologic examination of papillary tissue in urine in one, and on autopsy findings in the rest. Papillary necrosis was bilateral in three-fourths of the cases. The clinical picture varied. Most of the patients (67%) presented with chills and fever. Flank pain and dysuria were present in 11 patients (41%). As a rule oliguria was rare and progressive uremia was uncommon. In cases diagnosed at post-mortem, the patients had succumbed to infection or to a primary severe extrarenal disorder with the possibility of RPN having been entertained clinically in only half these cases prior to autopsy.
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PMID:Renal papillary necrosis: an update. 703 74

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

This study sought to characterize patients with renal papillary necrosis seen at one tertiary referral center by reviewing medical records of patients with a confirmed diagnosis between January 1, 1976 and September 1, 1992. One hundred sixty-five cases were identified. The mean age at diagnosis was 57 yr (SD 15). The female-to-male ratio was 1.1:1.0. Ninety-two percent of patients were white. Seventy-seven percent of cases were unsuspected before diagnosis, and 16% were diagnosed at autopsy. The most common associated conditions were urinary tract infection, analgesic abuse, urinary tract obstruction, diabetes mellitus, and sickle cell disease. There was considerable overlap in the presence of these conditions, with two or more identified in 36% of patients. In addition, 11% of patients had none of these well-recognized risks. Other diagnoses in this group included lupus nephritis, Wegener's granulomatosis, and renal artery stenosis. A decline in case numbers of approximately 50% was demonstrated over the last 10 yr studied. This period was associated with a 57% reduction in the number of excretory urograms carried out, suggesting that changes in diagnostic imaging preference may have contributed. Vital status and renal outcome data after diagnosis were obtained in 93% of cases. Of those diagnosed while living, survival was lowest among diabetic patients. Ten-year survival for nondiabetics was not significantly different from the expected survival of an age- and sex-matched cohort. The overall risk for requiring renal replacement therapy after the diagnosis of renal papillary necrosis in surviving patients was low (7% of 136 patients at risk).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal papillary necrosis--a sixteen-year clinical experience. 757 92


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