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

Reduction of renal mass (11/12) in rats leads to progressive azotemia, proteinuria, and hypertension. Less extensive renal ablation resulting from uninephrectomy also accelerates the progression of focal glomerulosclerosis (FGS) induced by experimental diabetes, renal irradiation, aminonucleoside nephrosis, or aging. The consequence of the absence of one kidney in man are examined in three different clinical situations. Unilateral renal agenesis seems to predispose to the development of FGS, but most reports include isolated cases and the true incidence of FGS is not known. The solitary kidney following uninephrectomy for acquired unilateral disease undergoes a compensatory rise in glomerular filtration rate (GFR) that remains stable for several decades. Finally, kidney donors followed for over 2 decades show unimpaired GFR, elevated at 70% to 80% of the normal (two-kidney) GFR. Some donors develop mild, nonprogressive proteinuria. Their incidence of hypertension matches that in the control population. Thus, hyperfiltration secondary to 50% reduction of renal mass in humans does not lead to loss of function of the remaining parenchyma.
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PMID:The solitary kidney: a model of chronic hyperfiltration in humans. 277 30

Contrary to popular belief, the primary directive for the release of renin is not the preservation of circulatory homeostasis, since activation of this hormonal system in patients with chronic heart failure results in deleterious rather than beneficial effects on cardiac performance. Instead, renin appears to be released by the kidneys to maintain glomerular filtration rate when renal perfusion pressure is reduced. The renin-angiotensin system carries out this beneficial action by exerting a constrictor action on the efferent arteriole. In doing so, renal blood flow declines, but filtration fraction increases and thus, glomerular hydraulic filtration pressure (and renal function) is preserved, despite severe renal hypoperfusion. When the formation of angiotensin II is inhibited during converting-enzyme inhibition, the beneficial action of this hormone on the efferent arteriole is lost, and renal function may deteriorate. This sequence of events is most likely to be seen when four risk factors are present: hyponatremia; high-dose diuretic therapy; diabetes mellitus; and the use of long-acting converting-enzyme inhibitors. In randomized studies, renal insufficiency developed more frequently with enalapril and lisinopril than with captopril. This risk of worsening azotemia is particularly high in patients with the most severe (class IV) heart failure.
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PMID:Identification of risk factors predisposing to the development of functional renal insufficiency during treatment with converting-enzyme inhibitors in chronic heart failure. 267 Feb 21

In a prospective study of all patients with Pseudomonas pseudomallei infections admitted to a large provincial hospital in northeastern Thailand, 63 cases of septicemic melioidosis and 206 patients with other community-acquired septicemias were documented during a 1-y period. Apart from P. pseudomallei, the spectrum of bacteria isolated from blood cultures and the overall mortality (32%) were similar to those previously reported elsewhere. Death from septicemia was associated with failure to develop a leukocytosis or pyrexia over 38 degrees C, azotemia, hypoglycemia, and jaundice. Septicemic melioidosis presented mainly in the rainy season, occurred predominantly in rice farmers or their families, and was significantly associated with preexisting diabetes mellitus or renal failure (P = .03). Blood-borne pneumonia and visceral abscesses were common and the mortality was high (68%; P less than .001). The response to appropriate treatment was slow (median fever clearance time 5.5 d) and the median duration of hospital stay was 4 w. Septicemic melioidosis is a major cause of morbidity and mortality in northeast Thailand.
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PMID:Melioidosis: a major cause of community-acquired septicemia in northeastern Thailand. 270 42

In four adults with idiopathic nephrotic syndrome and azotemia, percutaneous renal biopsy showed diabetic glomerulosclerosis, yet none had oral glucose tolerance tests diagnostic of diabetes mellitus or funduscopic evidence of diabetic retinopathy. Possible concomitant glomerular disease that may have produced proteinuria was excluded. Well documented cases of diabetic glomerulosclerosis without concurrent glucose intolerance are uncommon, and almost 30% of such patients have a past history of diabetes. Despite the absence of overt diabetes at onset of diabetic glomerulosclerosis, these patients warrant careful monitoring of plasma glucose levels and strict control of systemic hypertension.
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PMID:Diabetic glomerulosclerosis without concurrent diabetes mellitus. 305 23

The nephropathy complicating insulin-dependent diabetes mellitus (IDDM) has been well studied, but that complicating non-insulin-dependent diabetes mellitus (NIDDM) is less well defined. In patients with IDDM, the glomerular filtration rate is often increased early in the course of the disease, approaches normal with insulin therapy, but tends to remain slightly elevated throughout the ensuing 10-15 yr of insulin dependency. After the onset of overt azotemia, end-stage renal disease (ESRD) develops in approximately 5 yrs. Proteinuria may be intermittently positive in the earliest stages of diabetes, evolving into intermittent and then persistent microalbuminuria, which in turn blossoms into macroalbuminuria. Because 40-50% of IDDM patients develop proteinuria and two-thirds of this subpopulation develop ESRD, some 20-30% of any given cohort of IDDM patients eventually need dialysis or transplantation. Evidence indicates that diabetic nephropathy is associated with a greater incidence of eye, nerve, heart, and peripheral vascular disease. Nondiabetic renal disease complicating IDDM and NIDDM is associated with a lesser frequency and severity of these extrarenal manifestations. The prevalence of retinopathy increases with advancing nephropathy. Roughly two-thirds of the deaths from IDDM are related to renal failure, and most of the remainder are caused by associated cardiovascular disease. Transplantation from living relatives carries the best prognosis for survival, and little difference is seen between hemodialysis, peritoneal dialysis, and cadaver transplantation. The health-care costs of treating diabetic nephropathy are also reviewed.
Diabetes Care
PMID:Clinical features and health-care costs of diabetic nephropathy. 307 74

A total of 125 patients with severe peripheral vascular disease were examined with translumbar aortography. The mean dose of contrast medium injected was 65 ml of Angio Conray (containing 31.2 g of iodine). Forty patients were pretreated with mannitol, and 32 received furosemide. Thirty-eight patients (30%) had diabetes and, presumably, diabetic nephropathy. Eleven of them had significant azotemia (creatinine values greater than or equal to 4 mg/dl). Administration of contrast material did not significantly reduce renal function in any patient group. We conclude that acute renal failure following the injection of contrast material is uncommon, is reversible, and almost always occurs when avoidable complicating factors are present.
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PMID:Contrast media for angiography: effect on renal function. 307 23

A 51-year-old man with diabetes mellitus and mild hypertension developed acute interstitial nephritis 4 days after starting a course of co-trimoxazole for bronchopneumonia. Following initial symptoms of overt hypersensitivity, he developed azotemia and renal tubular dysfunction with malaise and anorexia requiring hospitalization. Renal pathology demonstrated an acute granulomatous interstitial nephritis superimposed on chronic diabetic renal disease.
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PMID:Acute granulomatous interstitial nephritis due to co-trimoxazole. 326 85

Changes in the choroidal artery were examined at autopsy in 16 Japanese patients with hypertension and insulin-dependent diabetes mellitus. These changes could be divided into 1) arteriosclerotic ones consisting of intimal thickening due to migration of smooth muscle cells, 2) hyaline deposits in the subendothelium, 3) extensive degeneration (moth-eaten atrophy and necrosis) of medial smooth muscle cells, and 4) changes resulting from fibrinoplatelet thrombi and their organization (recanalization and obstruction). The intimal thickening and medial damage correlated with aging, were accelerated by hypertension, and were remarkable in arterioles less than 60 micron in diameter. Diabetes mellitus apparently did not enhance these vascular changes. Thrombotic occlusion or narrowing of the choroidal artery was frequently observed in the arterioles of patients with hypertension and diabetes mellitus who had chronic azotemia or renal insufficiency. Subendothelial hyaline deposits were increased in patients with diabetes. The narrowing or obstructive changes in the choroidal artery were extensive in the intraocular blood vessels. These changes may be secondary and induce damage to other intraocular blood vessels and tissues, including the retina.
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PMID:Clinical choroidal thrombosis, hypertension, and diabetes mellitus: an electron microscopic study. 333 93

In vitro platelet aggregometry was performed in 201 patients with diabetes mellitus, and in 106 controls. The complication-free and retinopathic patients showed hyperaggregability to collagen and arachidonic acid, and also to epinephrine and adenosine diphosphate when neuropathy occurred. Patients with nephropathy, both with and without azotemia, had diminished in vitro platelet responses to each of the four stimuli as compared to age- and sex-matched controls. These characteristics were independent of the type of diabetes. It is concluded that diabetic nephropathy is characterized by reduced platelet in vitro reactivity. Further research is necessary to explain in vitro hypoaggregability in contrast to the numerous proofs of in vivo hyperfunction of platelets in diabetes.
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PMID:Platelet hyper- and hypoaggregability in different microangiopathic complications of diabetes mellitus. 340 79

In early stages of permanent renal injury or extensive ablation, structural and functional adaptations associated with hypertrophy partially compensate for nephron losses. Glomerulotubular balance is maintained in these conditioned nephrons by intrinsic tubule and peritubular capillary adaptations that parallel single nephron glomerular filtration rate (SNGFR). Studies of Na+-H+ exchange in renal cortical brush border membrane vesicles indicate that tubule functional adaptation is not tied to loss of renal mass per se but rather to factors such as dietary protein content that set the level of SNGFR. Likewise, the structural heterogeneity that follows chronic renal injury or extreme ablation of renal mass is less a consequence of nephron injury than of adaptation linked to dietary protein intake. Indeed, since dietary protein restriction blunts the need for compensatory glomerular hyperfiltration, there is neither a stimulus for nephron hypertrophy nor for enhanced tubule ion and fluid transport. In rats with remnant kidneys, experimentally induced diabetes mellitus, or severe hypertension, increases in glomerular pressures and flows precede proteinuria, glomerular sclerosis, and azotemia. Protein restriction prevents these hemodynamic adaptations as well as the late complications. Similar conclusions appear to be applicable to a wide spectrum of clinical circumstances characterized by reduced nephron number.
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PMID:Nephron adaptation to renal injury or ablation. 389 71


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