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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal microvasculature was examined stereoscopically after intraarterial injection of silicone rubber. Specimens studied were: 29 cases of normal kidney, 4 cases of sclerotic kidney, 10 cases of acute renal failure, and 10 cases of chronic renal failure from the final stage of chronic glomerulonephritis, malignant nephrosclerosis, diabetic nephropathy, and cortical necrosis. The following were common evidences for chronic renal failure: much reduction and wide deficiencies of filling in the cortex, increased filling of vasa recta, narrowing and spiralling of interlobular arteries and cortical afferent arterioles, appearance of giant glomeruli, rarefaction of the peritubular capillary plexus, and relative preservation of glomeruli in the juxtamedullary zone and vasa recta in the medulla may be the major pathway, after the interlobular arteries and afferent arterioles in the subcapsular cortex are destroyed, and these vascular architectural changes may be intimately related to the pathophysiology of chronic renal failure.
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PMID:Renal microvasculature in chronic renal failure. 106 90

The course and prognosis of chronic renal failure are much worse in hypertensive patients than in normotensive patients with otherwise similar basic disease. Therefore, antihypertensive measures with a combination of diuretics, beta-blockers, and vasodilators have clearly been shown to improve the progression of diabetic nephropathy. Treatment of hypertension with angiotensin-converting enzyme (ACE) inhibitors has also been shown to have a favorable effect on the prognosis of chronic renal failure. In the past few years, more knowledge about the pathogenesis of hypertension and the development of hypertension-induced organ damage has been followed by changing attitudes to antihypertensive therapy and the introduction of calcium antagonists for the treatment of hypertension, even in chronic renal failure. ACE inhibitors and calcium antagonists seem to be advantageous in the prognosis of chronic renal failure as they act on the humoral and trophogenic factors now known to be important in antihypertensive therapy.
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PMID:The effect of antihypertensive therapy on the course of renal failure. 128 93

Diabetes mellitus can lead, along the years of its course, to chronic renal failure in a high proportion of cases. An early risk-indicator of later diabetic nephropathy is the presence of microalbuminuria, but it usually takes about fifteen to twenty years to appear. Before that, no clinical signs can disclose the underlying alterations of glomerular basement membrane that will eventually bring forth overt nephropathy. The usefulness of the altered excretion of isoenzymes of amylase as an early marker of the glomerular charge selectivity was tested in 202 juvenile onset insulin-dependent diabetics, compared with 51 normal subjects matched for age and sex. The diabetic patients studied showed increased excretion of salivary amylase into urine. The salivary to pancreatic amylase ratio of concentrations in urine was always below 1 in normal subjects, and was increased over 1 in 33.2% of diabetics, although microalbuminuria was present only in 26.2% of patients. The excretion of other proteins was within reference values in the majority of cases, indicating that the kidney was not seriously affected in those patients. Moreover, the altered salivary to pancreatic amylase ratio in urine was more prevalent than microalbuminuria (36.6% vs 18%) in the first decade of the evolution of the diabetes. These results indicate that the ratio of excretions of both isoamylases into urine is a more sensible and earlier marker of altered glomerular charge barrier for anionic proteins.
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PMID:Utility of filtration markers to monitor the quality of glomerular function. 128 36

The incidence of end-stage renal disease is increasing and this results in an enhanced requirement of renal replacement therapy facilities. This brings about a significant burden on health care budgets and makes strategies that slow down or even prevent deterioration of the renal function mandatory. Although large scale randomized, controlled and prospective clinical trials on the effect of blood pressure control on the course of renal function are lacking, there is circumstantial evidence from animal, epidemiological and clinical studies to state that treatment of hypertension to blood pressure values well within the normal range is most important to ameliorate the downhill course of renal function in patients with chronic renal failure. Moreover, treatment of hypertension is critical to reduce morbidity and mortality of cardiovascular disease in these patients, who have an increased risk for such events. Low-protein diets, if possible with ketoacid supplement, are advocated to slow down the deterioration of renal function. However, based on the results of recent studies, low-protein diets may only have a moderate effect in patients with diabetic nephropathy and, possibly, in patients with chronic glomerulonephritis. The possibility of influencing renal ammoniagenesis by protein restriction or calcium carbonate administration, and an attenuation of alternative complement pathway activation and tubulo-interstitial injury, are challenging. Finally, in animal studies it has been found that abnormalities in serum lipid profile contribute to the progression of chronic renal failure, which may be prevented by pharmacological treatment of hyperlipidemia. Studies in humans concerning this subject are lacking at this moment, but treatment of hyperlipidemia is proper to reduce cardiovascular events.
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PMID:Clinical strategies for arresting progression of renal disease. 140 61

A 66-year-old white man presented with severe chronic renal failure. He had no past or present symptomatic glucose intolerance nor a family history of diabetes mellitus. Several fasting plasma glucose determinations, hemoglobin Alc and an oral glucose tolerance test were normal. Funduscopic ophthalmoscopy and retinal fluorescein angiography did not demonstrate diabetic retinopathy. The kidney biopsy showed nodular diabetic nephropathy, with increased mesangial matrix, thickened glomerular basement membrane, and afferent and efferent glomerular arteriolar hyalinization. The diagnosis of nodular diabetic nephropathy was made in this patient in the absence of past or present or familial evidence of diabetes mellitus.
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PMID:Nodular diabetic glomerulosclerosis without diabetes mellitus. 143 40

This article encompasses the topic of dietary impact upon the diabetic individual with the condition of diabetic nephropathy. The influence of diet will be addressed in: renal insufficiency, chronic renal failure, and the modalities of hemodialysis, peritoneal dialysis, and renal transplantation. The two-fold purpose of this review is to provide documentation in support of dietary therapy and to underscore the sharp contrast in nutritional needs dependent upon the individual's clinical status.
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PMID:Dietary modifications: impact on diabetic nephropathy. 145 90

With the aim of determining the relative prevalence of the diseases underlying chronic renal failure (CRF) in a large homogeneous black tropical population, the autopsy records of the Obafemi Awolowo University Teaching Hospital over a four year period were studied. Out of a total of 702 cases coming to autopsy during this period, 66 (9.4%) died as a result of CRF. The highest number of cases of CRF fell within the 31-40 year age group with a male/female ratio of 1.28:1. Chronic glomerulonephritis was responsible for 40.9% of cases, malignant nephrosclerosis 16.6%, benign nephrosclerosis 7.6% while endstage renal disease (ESRD) was responsible for 15.4%. A miscellaneous group of diseases was responsible for 19.7%, about half of which was due to chronic pyelonephritis. Rarer causes of CRF were diabetic nephropathy, multiple myeloma, systemic lupus erythematosus and analgesic nephropathy.
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PMID:The pathological basis of chronic renal failure in Nigerians. An autopsy study. 149 21

Experimental animal studies have demonstrated a renal protective effect of ACE inhibition therapy in diabetes mellitus and the remnant kidney model of chronic renal failure. The mechanism of this effect is secondary, at least in part, to the drugs' effects on glomerular hemodynamics. In addition, there is further evidence to suggest that ACE inhibitors may influence other pathogenic mechanisms of progressive renal insufficiency. Preliminary data in clinical studies suggest that ACE inhibition therapy decreases proteinuria and may ameliorate the decline of the glomerular filtration rate in diabetic nephropathy and progressive renal insufficiency of other etiologies. However, before this conclusion can be definite, a large, prospective, randomized clinical trial is required to compare ACE inhibitors to conventional antihypertensive agents. Since calcium channel blockers are metabolically neutral in that they do not increase serum cholesterol or glucose levels and generally do not cause orthostatic hypotension, they may be ideal agents for such a comparison study.
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PMID:Progressive renal insufficiency: the role of angiotensin converting enzyme inhibitors. 155 7

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

We report here a case of penile gangrene in a patient with diabetic nephropathy treated by continuous ambulatory peritoneal dialysis (CAPD). The patient demonstrated severe systemic arteriosclerosis. The main cause of the gangrene was considered to be circulatory insufficiency induced by severe arteriosclerosis. Several predisposing factors including chronic renal failure, long-term diabetes mellitus and CAPD-related metabolic changes such as abnormalities of lipid metabolism also appeared to have contributed to the arteriosclerotic changes. The prognosis in cases of this type is thought to be extremely poor.
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PMID:Penile gangrene in a patient with diabetic nephropathy on continuous ambulatory peritoneal dialysis. 177 43


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