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A simple ultrasonic method was used for measuring transplanted kidney volume in 29 patients. Five of these patients developed diabetes mellitus and six women became pregnant following transplantation. Serial measurements were performed over periods of 6-12 months after transplantation. The kidney volume became stable 6 months after transplantation and this volume correlated positively with the renal function. Renal hypertrophy was noted in those transplant patients who developed diabetes mellitus following transplantation and this hypertrophy was associated with improvement in graft function. Transplant volume also rose in acute rejection and returned to normal after appropriate treatment. During pregnancy following transplantation, the transplant volume increased early in pregnancy to return to normal before delivery. This volume increase was also associated with graft function improvement.
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PMID:Changes in transplanted kidney volume measured by ultrasound. 330 2

Renal hypertrophy is a common consequence of diabetes mellitus that precedes and possibly accounts for the increased glomerular filtration rate. We have postulated that the glucose-mediated increase in the intracellular concentration of sodium [Na]i initiates the chain of events leading to the increase in cell size and eventually cell number. Experiments were conducted on Sprague-Dawley rats made diabetic by the intravenous injection of 45 mg/kg body wt of streptozotocin dissolved in a 5 mM citrate buffer solution. Control animals were injected with the vehicle alone. Ninety-six hours and 11 weeks later, measurements of [Na]i were done by NMR spectroscopy on suspensions of proximal tubules, using dysprosium tripolyphosphate as an extracellular shift reagent. At 96 hours after the induction of the diabetes, there was a 60% increase in [Na]i compared to control (P less than 0.01). No further increase in [Na]i was observed during the subsequent 11 weeks of observation. Addition of ouabain (1.0 mM) resulted in a fourfold increase in [Na]i in tubules from control animals, and a 2.5-fold increase in tubules from 96-hour diabetic rats. Ouabain-inhibitable Na+-K+-ATPase activity was substantially higher in the renal tubules of diabetic rats, the increase being proportional to that of [Na]i. In order to ascertain the effect of hyperglycemia on [Na]i, proximal tubules prepared from kidneys of normal and diabetic rats were exposed to low (5 mM) and high (25 mM) concentration of glucose in the media.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracellular sodium in proximal tubules of diabetic rats. Role of glucose. 338 34

Renal hypertrophy in rats with streptozotocin diabetes or after unilateal nephrectomy was studied by sterological techniques. -- After 4 days of diabetes total glomerular volume had increased by 30%, and after 47 days by 43%. Glomerular growth was more pronounced than whole kidney growth during the first 4 days, but subsequently whole kidney growth exceeded glomerular growth. In control rats glomerular volume was 4.9% of total kidney volume; after 4 days of diabetes it was 5.4% and after 47 days 4.1%. -- Proximal tubule length increased from 366 m/kidney in control rats to 447 m/kidney after 47 days of diabetes; tubular luminal diameter increased from 26.8 micrometer to 31.4 micrometer in the same rats. Tubular length and luminal diameter were, however, not increased after 4 days of diabetes. -- In unilaterally nephrectomised rats there was no early rapid glomerular growth. Glomerular fractional volume was 4.9% in controls, 4.4% at four days, and 4.2% at 24 days after nephrectomy. -- The results indicate a disturbed glomerulo-tubular balance in the early phases of diabetic renal hypertrophy.
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PMID:Renal hypertrophy in experimental diabetes. A morphometric study. 741 59

The role of ornithine decarboxylase (ODC) and polyamines in kidney hypertrophy is controversial. Since part of this controversy could be related to differences in the model system used by the different authors, we studied the changes in renal ODC and polyamines in six different models of kidney hypertrophy in mice, including compensatory renal hypertrophy produced by unilateral nephrectomy, experimental diabetes, potassium depletion and treatment with hormones such as testosterone, thyroxine and fluorocortisone. Only in the case of renal hypertrophy produced by testosterone administration was there a significant increase in ODC activity and putrescine content in the kidneys. However, the concomitant treatment with difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, as a 2% solution in the drinking water completely abolished the increase of renal ODC, but the kidney weights increased and other androgenic effects, such as the induction of renal beta-glucuronidase, were not affected. Moreover, DFMO-treatment did not prevent the kidney enlargement produced in other types of hypertrophy, even in the cases associated with hyperplasia. The present results support the premise that, at least in mice, the increase in ODC activity and polyamine biosynthesis is not required for kidney growth, and also that in most cases renal enlargement is not accompanied by any increase in the polyamine content.
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PMID:An evaluation of the role of polyamines in different models of kidney hypertrophy in mice. 747 58

IGF-I acts as a renotropic factor in early streptozotocin-induced diabetes. Somatostatin analogue (octreotide) treatment initiated at the onset of diabetes prevents kidney IGF-I accumulation and renal growth. Seven days of octreotide treatment initiated after 3, 5, 7 or 9 days of untreated diabetes was investigated. Diabetic renal hypertrophy was followed by renal hyperplasia. Compared with placebo-treated diabetic rats, the earliest octreotide intervention was followed by a greater reduction in renal growth compared with intervention later on (days 3 to 10, 12%; days 5 to 12, 10%; days 7 to 14, 9%; days 9 to 16, 6%; P < 0.05). Octreotide treatment was unable to reduce protein accumulation and kidney DNA increase consistently. No difference in glomerular volume fraction or total glomerular volume was observed between placebo- and octreotide-treated diabetic rats. Octreotide treatment was followed by reduced kidney and serum IGF-I especially following early intervention, while no effect over that of diabetes was observed in the later intervention periods. The results confirm the notion that initial renal IGF-I accumulation is a prerequisite for early diabetic kidney hypertrophy in rats and show that delayed octreotide treatment cannot reverse renal and glomerular growth which is already manifest.
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PMID:Effect of octreotide on experimental diabetic renal and glomerular growth: importance of early intervention. 749 May 42

Formation of polyamines has previously been shown to play an important role for initial kidney growth in experimental diabetes, as treatment of diabetic rats with a selective ornithine decarboxylase (ODC) inhibitor, initiated immediately after diabetes induction, abolishes the initial kidney growth. In order to investigate the role of polyamine formation for the maintenance of diabetic kidney hypertrophy, ODC inhibition was initiated after manifest kidney hypertrophy had occurred. The kidney weight in diabetic rats was significantly larger than in control rats after a diabetes duration of 7, 14, 50 and 71 days and the total glomerular volume was increased in kidneys from diabetic rats after a diabetes duration of 71 days. Renal activity of ODC was increased in diabetic rats throughout the study period of 71 days. Treatment of diabetic rats with the selective ODC inhibitor di-fluoro-methyl-ornithine (DFMO) was maintained for two periods (days 7-14 and days 50-71). DFMO treatment had no effect on 24-h food consumption, blood glucose concentration or body weight. However, despite almost total inhibition of the kidney ODC activity, there was no effect on kidney growth or total glomerular volume in the DFMO treated diabetic rats compared to placebo treated diabetic rats. Finally, the urinary albumin excretion was markedly increased in diabetic rats with no effects of ODC-inhibition. In conclusion, inhibition of ODC initiated in diabetic rats with manifest kidney enlargement had no effect on renal size, glomerular volume or urinary albumin excretion. These findings together with our previous findings indicate that the role of polyamines in diabetic kidney enlargement is restricted to the first week after diabetes induction.
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PMID:Inhibition of renal ornithine decarboxylase activity fails to reduce kidney size and urinary albumin excretion in diabetic rats with manifest kidney hypertrophy. 779 31

Renal hypertrophy is an early feature of diabetes, and it may predispose the kidney to the eventual development of parenchymal dysfunction. Since we have previously demonstrated that short-term culture in high glucose concentration stimulates production of transforming growth factor-beta 1 (TGF-beta 1) in proximal tubular and glomerular mesangial cells, we postulated that this cytokine, which has potent regulatory effects on cellular growth and extracellular matrix production, is important in mediating diabetic renal disease. In this study we evaluated the gene and protein expression of TGF-beta 1 in the kidney of two rodent models of spontaneous insulin-dependent diabetes mellitus [the biobreeding (BB) rat and the nonobese diabetic (NOD) mouse]. In association with the appearance in both models of significant renal hypertrophy, TGF-beta 1 mRNA levels were increased threefold in the kidney of the diabetic BB rat after 3 days of diabetes and also threefold after 7-9 days in the NOD mouse. There was no increase in TGF-beta 1 transcripts in the livers of the diabetic animals, suggesting that this response is tissue specific. Immunohistochemical studies revealed that TGF-beta 1 protein is concordantly elevated in the cortical tubular cells of the diabetic kidney in both models. These results suggest that the stimulated expression of renal TGF-beta is an early manifestation of the involvement of the kidney by diabetes. Whether increased TGF-beta production in the diabetic kidney is a key promoter of diabetic renal manifestations (e.g., hypertrophy) deserves additional studies.
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PMID:Renal hypertrophy is associated with upregulation of TGF-beta 1 gene expression in diabetic BB rat and NOD mouse. 781 Jun 96

Renal hypertrophy in diabetes is accompanied by an increase in kidney protein content, which reflects an imbalance between protein synthesis and degradation. This study determines whether altered cellular protein degradation contributes to the imbalance. Diabetes was induced in rats with streptozotocin (55 mg/kg/ip). After 2 or 4 days of diabetes, kidney weight and protein content were measured. Over the 4 days, despite a loss in body weight, kidney wet weight increased by 35% and protein content by 37% in the diabetic rats. Treatment with insulin prevented this increase. Long-lived protein degradation was measured in isolated proximal tubules prelabeled with (14C)valine in vivo. Two days after streptozotocin, protein degradation was depressed by 19% (P < 0.05) and by the fourth day by 27% compared with that in nondiabetic controls (2.6% +/- 0.2 versus 1.9 +/- 0.1% degraded/h; P < 0.01). This was accompanied by a similar diabetes-induced decrease in proximal tubule cathepsin B and L activity. Accordingly, this study provides direct evidence that, in diabetes, tubular cell protein breakdown is depressed and suggests that altered lysosomal cathepsin activity may contribute to this effect. Depressed proteolysis likely contributes to the increase in kidney protein content and hence to diabetic renal hypertrophy.
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PMID:Tubular cell protein degradation in early diabetic renal hypertrophy. 802 32

Ingestion of a high-protein diet or intravenous administration of amino acids is associated with an increase in glomerular filtration rate (GFR). It can also lead to renal hypertrophy, and, if sustained, may cause glomerular sclerosis. L-Arginine administration ameliorates the progression of renal disease in rats with subtotal nephrectomy and prevents the increase in GFR observed in rats with experimental diabetes. The present study examines the potential effect(s) of L-arginine administration (1%) in the drinking water on the renal hypertrophy that occurs in rats fed a high-protein diet for 1 month. Four groups of female Sprague-Dawley rats, six in each group, were studied (95 +/- 1 g). Groups 1 and 2 were fed a low-protein diet (12% casein, 0.504% L-arginine); Group 1 was given tap water, whereas Group 2 was given tap water supplemented with L-arginine. Groups 3 and 4 were fed a high-protein diet (40% casein, 1.68% L-arginine); Group 3 was given tap water, whereas Group 4 was given tap water supplemented with L-arginine. The rats had free access to food and water during the study period. The kidney weight and the kidney to body weight ratio of rats of Group 3 were significantly greater than in the other groups of rats. Renal hypertrophy was prevented in the rats of Group 4. The excretion of orotic acid in the urine, an index of L-arginine deficiency, was significantly greater in rats of Group 3 than in rats of Group 4. Thus, the renal hypertrophy that occurs in rats fed a high-protein diet was decreased in rats given L-arginine supplementation in the drinking water. This effect was associated with less excretion of orotic acid in the urine in rats given L-arginine. A relative deficiency of L-arginine may occur during high-protein feeding that may shunt nitrogen metabolism from the urea cycle to the orotic acid pathway.
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PMID:Dietary supplementation of L-arginine ameliorates renal hypertrophy in rats fed a high-protein diet. 820 40

Renal hypertrophy and elevated glomerular filtration rate (GFR) appeared in early stage of diabetic nephropathy (DN). In order to investigate the effect of Rheum officinale (RO) on the renal hypertrophy, streptozotocin induced diabetic rats with moderate hyperglycemia were divided into two groups, receiving RO (RO-DN) or not (DN), and one group of non-diabetic control (C) was set up. At the 28th day, DN group exhibited heavier kidney weight (+61%), more protein (+133%) and DNA (+94%) contents in the kidney and higher GFR (+94%) than the control. RO-DN rats showed much less above mentioned changes. In addition, lipid abnormalities were ameliorated in RO-DN group. This result suggest that RO is beneficial to the diabetes in terms of renal hypertrophy and GFR changes at early stage and is recommended in the treatment of diabetic nephropathy.
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PMID:[Effects of Rheum on renal hypertrophy and hyperfiltration of experimental diabetes in rat]. 821 81


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