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

Micropuncture studies were made on insulin-treated streptozotocin diabetic rats two weeks after the induction of diabetes and on age-matched control rats. Kidney size, GFR and single nephron GFR were higher in poorly controlled diabetic rats than in normal animals. Single nephron GFR rose as a result of an increase in the hydraulic pressure difference across the glomerular capillary wall caused mainly by a rise in the glomerular capillary pressure due to a diminished ratio of afferent to efferent arteriolar hydraulic resistances. Furthermore, the intratubular pressure was reduced as a result of a decrease in hydraulic resistance in the loop of Henle. Strict metabolic control prevented these changes. In conclusion, the increase in renal function in experimental diabetes is determined by the degree of metabolic control excluding a potential nephrotoxic effect of streptozotocin per se.
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PMID:Strict metabolic control and renal function in the streptozotocin diabetic rat. 355 Feb 16

Relative low serum levels of parathormone (PTH) and low incidence of secondary hyperparathyroidism have been reported in diabetic uremic patients. The pathogenesis of this reported resistance to uremic secondary hyperparathyroidism in diabetes remains controversial. We have measured the serum C-terminal parathormone (C-PTH) renal phosphorus threshold (TmPO4) and nephrogenous cyclic AMP (N-cCAMP), in 2-hour urine collection in 22 patients with diabetic nephropathy with moderate chronic renal failure and in 27 controls with similar creatinine clearance values (18.16 +/- 9.14 and and 19.1 +/- 8.47 ml/min). In spite of the lower levels of serum C-PTH (1.07 +/- 0.43 ng/ml) diabetic patients exhibited an increased phosphaturia (TmPO4: 1.97 +/- 0.9 mg/100 ml GFR) when compared with the control group (C-PTH: 2.01 +/- 1.17 mg/ml, and TmPO4: 2.5 +/- 0.7 ml GFR). When the C-PTH values were plotted against the logarithm of creatinine clearance values, both groups showed a significant linear relationship reflecting the progressive increase in PTH when GFR fell. This progressive parathyroid stimulus was also present in diabetic patients but in a lower intensity. We believe that increased phosphaturia in diabetics with moderate chronic renal failure may be a major factor in precluding the appearance of secondary hyperparathyroidism in these patients once they reach the dialysis and transplantation programs.
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PMID:Relative hyperphosphaturia in diabetic chronic renal failure: a protective factor of hyperparathyroidism. 367 Feb 26

103 Indians (74 females, 29 males) with NIDDM diagnosed before age 30 yr on the basis of the revised WHO diagnostic criteria were studied in order to assess the prevalence of microvascular complications. The mean duration of NIDDM in the subjects was 11 yr (range 2-38 yr). 24 patients (23%) eventually required insulin therapy for control after a mean interval of 11.8 yr (range 5-38 yr). Diabetic retinopathy was present in 37 patients (35.9%), of whom 6 had proliferative retinopathy. Nephropathy was found in 16 patients (15.5%). The mean GFR of these patients was 46.8 ml/min, compared to a mean of 97.1 ml/min in 12 of the patients without nephropathy who had a similar mean duration of disease. The mean duration of disease in patients with retinopathy and nephropathy was 14.9 yr and 14.8 yr respectively. In the patients who eventually required insulin therapy both retinopathy (75%) and nephropathy (41%) were more common but the mean duration of disease in these patients was longer (16 yr vs 9 yr). This study has underlined the heterogeneity of NIDDM in the young, as microvascular complications are by no means uncommon in South African Indians with the disease.
Diabetes Res 1986 Nov
PMID:Microvascular complications and non-insulin-dependent diabetes of the young in South African Indians. 382 87

Forty percent of patients with insulin-dependent diabetes will develop nephropathy during the course of their disease, thus being the most important single disorder leading to end-stage renal failure (ESRF). Intensive metabolic control delays onset of diabetic nephropathy, the first omen of which is appearance of subclinical albuminuria, also termed microalbuminuria. Moreover, it is now established that intensive treatment of hypertension reduces rate of decline in GFR and thus postpones ESRF. When uremia eventually sets in, a range of biochemical and endocrine abnormalities can be included among those characteristics of diabetes mellitus per se. These include elevated plasma levels of growth hormone, glucagon and free fatty acids, which may participate in the uremic insulin resistance superimposed on the preexisting diabetic carbohydrate intolerance. Hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) are two established modalities of renal replacement therapy in diabetes mellitus. Controlled clinical trials for comparison of CAPD versus HD treatment of diabetics are, however, still needed. The survival rate is approximately 80 and 65-95% in insulin-dependent diabetic patients at 1 year during treatment with HD and CAPD, respectively. However, it is general experience that diabetics on CAPD exhibit a glycemic control, superior to that attained during HD. It has not been proved that patient survival after cadaveric renal transplantation is better than on dialysis. The degree of vascular heart disease seems to be the major determinant for survival of kidney-transplanted diabetic patients.
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PMID:End-state renal failure in diabetic nephropathy: pathophysiology and treatment. 391 47

The purpose of our prospective study was to evaluate the long-term effect of aggressive antihypertensive treatment on glomerular filtration rate and albuminuria in young female and male patients with insulin-dependent diabetes mellitus with diabetic nephropathy and blood pressure greater than 90 mm Hg. Eight patients received treatment with metoprolol (200-400 mg/day), hydralazine (100-200 mg/day), and furosemide (80-500 mg/day). The untreated control group consisted of eight patients matched for age (mean 32 years), diabetes duration (mean 17 years), and sex (two female and six male patients). All patients except one had diabetic retinopathy. Glomerular filtration rate was measured after a single intravenous injection of 51Cr-labeled ethylenediaminetetraacetic acid. Urinary albumin concentration was determined with a radial immunodiffusion method. The investigations were performed two to four times per year in each patient. The mean observation period was 59 and 27 months in the treated and untreated groups respectively. Due to a considerable rise in arterial blood pressure, it was considered unethical to prolong the observation in the untreated group. Arterial blood pressure rose from 140/96 +/- 4/1 to 150/100 +/- 3/2 mm Hg; albuminuria increased from 1517 +/- 502 to 1911 +/- 120 micrograms/min; and glomerular filtration rate decreased by a mean of 0.84 +/- 0.17 ml/min/mo in the untreated group. Antihypertensive treatment induced blood pressure reduction 151/100 +/- 3/2 to 131/87 +/- 2/1 mm Hg; diminished albuminuria 1467 +/- 515 to 729 +/- 65 micrograms/min; and caused a slow rate of decline in GFR, mean 0.37 +/- 0.08 ml/min/mo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of long-term antihypertensive treatment on kidney function in diabetic nephropathy. 407 29

Renal sodium handling and microsomal Na+-K+-ATPase activity in kidney cortex, medulla and papilla of rats with streptozotocin-induced diabetes mellitus (DM) was studied. During 7 days following the administration of streptozotocin GFR, urinary excretion, filtered load and tubular reabsorption of Na+ averaged (mean +/- SE) 1.18 +/- 0.016 ml/min, 1.74 +/- 0.14, 177.3 +/- 8.9 and 175.6 +/- 8.9 mEq/min respectively in experimental rats as compared to corresponding rates of 0.85 +/- 0.04 (P less than 0.001), 0.85 +/- 0.03 (P less than 0.001), 129.8 +/- 5.8 (P less than 0.001) and 129 +/- 5.8 (P less than 0.001) respectively in the control rats. The activity of microsomal Na-K-ATPase in the kidney cortex, medulla and papilla of the control group was (mean +/- SE) 44.7 +/- 1.7, 150 +/- 7.5 and 37.4 +/- 3.6 (mumoles Pi/mg prot/h) respectively. 24 h after DM induction Na-K-ATPase activity in the cortex rose to 59.3 +/- 2.4 (P less than 0.001) and remained high after 3 and 7 days. Medullary Na-K-ATPase activity was unchanged 24 h after streptozotocin administration but was markedly increased to 260 +/- 9 (P less than 0.001) after 3 days and remained high after 7 days. These findings show that streptozotocin-induced DM in rats causes a substantial increase in GFR which is associated with a net increase in filtered and reabsorbed load of Na+ and natriuresis. These alterations are accompanied by a marked increase in Na-K-ATPase activity in renal medulla and in the cortex.
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PMID:The effect of streptozotocin-induced diabetes mellitus on urinary excretion of sodium and renal Na+-K+-ATPase activity. 608 93

The authors present a contemporary picture of the pathogenesis and clinical course of diabetic nephropathy in type I diabetics describing the stages of the disease and the possible evidence for reversibility of the kidney damage with tight metabolic control. During the so-called latency period, which is clinically non-detectable, the predominant functional abnormalities (increase in GFR with sub-clinical glomerular proteinuria) can be corrected by strict control although there is no evidence for the regression of the associated anatomical changes such as the enlarged filtration area. As for the described increase in thickness of the glomerular basement membrane, from experimental data and pancreatic transplants in man, delay in its development and to some extent regression of the glomerular lesions can be expected. The problem of how the renal lesions in experimental diabetes mirror the changes in the human kidney is discussed. During the symptomatic period, with intermittent and subsequently constant proteinuria and progressive decline in renal function, which are observed in only about 30% of type I diabetics, the role of arterial hypertension and its effective control is emphasized. Finally, the renal failure period is indicative of irreversible damage to the kidneys. The progression from its early to its late stages is variable between different patients but each individual patient shows a constant rate of deterioration. The evidence for the efficacy of medical treatment in slowing down its progression is very limited at present but much can be done to improve the quality of life by dietary measures, treatment of fluid overload and hypertension. When the end-stage diabetic kidney disease is reached, with serum creatinine above 8 mg/dl, renal transplantation from a living donor offers a good chance for a relatively acceptable quality of life for years. In conclusion, it is stressed that the morbidity of diabetic nephropathy could eventually be reduced through effective control of the metabolic abnormalities of diabetes with the methods presently available.
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PMID:The natural history of diabetic nephropathy in type I diabetes and the role of metabolic control in its prevention, reversibility and clinical course. 634 25

The earliest manifestations of clinical diabetic nephropathy, including proteinuria, hypertension, and declining GFR, represent very advanced diabetic glomerulopathy with especially prominent mesangial expansion. Mesangial expansion, by restricting glomerular capillary filtration surface and lumenal volume, stimulates compensatory mechanisms analogous to those resulting from a marked reduction in nephron number. These compensatory mechanisms involve alterations in glomerular hemodynamics designed to maintain glomerular filtration but which ultimately injure the kidney. These hemodynamic perturbations are not specific to diabetes but represent a final common pathway toward endstage renal failure that also characterizes the remnant kidney. This thesis concludes that the onset of clinical diabetic nephropathy augurs inevitable decline in kidney function, and that only studies and interventions exercised before clinical nephropathy develops can influence understanding and outcome of diabetic nephropathy.
Diabetes 1983 May
PMID:Diabetic nephropathy. A perspective. 640 Jun 68

Alterations in renal function and structure are found even at the onset of diabetes mellitus. Studies performed over the last decade now allow definition of a series of stages in the development of renal changes in diabetes. Such a classification may be useful both in clinical work and in research activities. Stage 1 is characterized by early hyperfunction and hypertrophy. These changes are found at diagnosis, before insulin treatment. Increased urinary albumin excretion, aggravated during physical exercise, is also a characteristic finding. Changes are at least partly reversible by insulin treatment. Stage 2 develops silently over many years and is characterized by morphologic lesions without signs of clinical disease. However, kidney function tests and morphometry on biopsy specimens reveal changes. The function is characterized by increased GFR. During good diabetes control, albumin excretion is normal; however, physical exercise unmasks changes in albuminuria not demonstrable in the resting situation. During poor diabetes control albumin excretion goes up both at rest and during exercise. A number of patients continue in stage 2 throughout their lives. Stage 3, incipient diabetic nephropathy, is the forerunner of overt diabetic nephropathy. Its main manifestation is abnormally elevated urinary albumin excretion, as measured by radioimmunoassay. A level higher than the values found in normal subjects but lower than in clinical disease is the main characteristic of this stage, which appeared to be between 15 and 300 micrograms/min in the baseline situation. A slow, gradual increase over the years is a prominent feature in this very decisive phase of renal disease in diabetes when blood pressure is rising. The increased rate in albumin excretion is higher in patients with increased blood pressure. GFR is still supranormal and antihypertensive treatment in this phase is under investigation, using the physical exercise test. Stage 4 is overt diabetic nephropathy, the classic entity characterized by persistent proteinuria (greater than 0.5 g/24 h). When the associated high blood pressure is left untreated, renal function (GFR) declines, the mean fall rate being around 1 ml/min/mo. Long-term antihypertensive treatment reduces the fall rate by about 60% and thus postpones uremia considerably. Stage 5 is end-stage renal failure with uremia due to diabetic nephropathy. As many as 25% of the population presently entering the end-stage renal failure programs in the United States are diabetic. Diabetic nephropathy and diabetic vasculopathy constitute a major medical problem in society today.
Diabetes 1983 May
PMID:The stages in diabetic renal disease. With emphasis on the stage of incipient diabetic nephropathy. 640 Jun 70

To study the renal hemodynamic response to a large intravenous bolus of a radiocontrast agent, 8 ml/kg body weight of 60% diatrizoate meglumine (D-60) was infused over 30 seconds in both normal rats and rats with streptozotocin-induced diabetes. The effect of equiosmolar mannitol (1350 mOsm/kg) was compared with the D-60 response in normal rats to examine the potential role of hypertonicity in mediating a response. A similar two-phase response was seen in all three groups. The effect of D-60 in normal rats was similar to that of mannitol, but all responses were reduced in diabetic rats. During Phase I in normal rats in response to D-60 there was a transient three-minute reduction in blood pressure (BP), and renal blood flow (RBF) fell by 62 +/- 7%. During Phase II blood pressure did not change from normal baseline values, but RBF fell by 29 +/- 5%; GFR fell by 42 +/- 3%, and filtration fraction (FF) diminished. In diabetic rats baseline FF was lower than normal and was not further reduced after infusion of D-60. It is suggested that D-60 reduces RBF and GFR by a nonspecific osmotic effect, perhaps related to tubuloglomerular feedback or to an acute increase in intratubular pressure. Responses to these mechanisms may be reduced in diabetic rats with a chronic glycosuric osmotic diuresis.
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PMID:The renal hemodynamic response to diatrizoate in normal and diabetic rats. 641 44


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