Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 64-year-old man was admitted because of abdominal fullness, edema and anorexia. He had come to our hospital for treatment of liver cirrhosis and diabetic nephropathy for 1 year. We started diuretics and human albumin intravenous administration. Although the edema disappeared and abdominal fullness improved a little, blood urea nitrogen (BUN) and serum creatinine became elevated, hepatic function deteriorated and he lost his appetite. We consequently started continuous ambulatory peritoneal dialysis (CAPD) in order to control ascites and uremia. Abdominal fullness, appetite and BUN and serum creatinine improved without hepatic function deterioration. It might be important to start CAPD to control ascites although serum creatinine levels might be slightly elevated.
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PMID:A case report of a diabetic nephropathy patient with cirrhotic ascites treated by peritoneal dialysis. 1730 79

Diabetic nephropathy (DN) is one of the main causes of end stage renal disease (ESRD) and a leading cause of diabetes mellitus related morbidity and mortality. Recently, sirtuin are reported to have emerging pathogenetic roles in cancer, muscle differentiation, heart failure, neurodegeneration, diabetes and aging. The aim of the present study was to study the role of intermittent fasting (IF) on DN and studying the expression of Sir2 and p53. At biochemical level, we found that IF causes significant improvement in blood urea nitrogen (BUN), creatinine, albumin and HDL cholesterol, parameters that are associated with the development of DN. Diabetic rats on IF also show significant improvement in onset of hypertension. Interestingly, the expression of Sir2, a NAD dependent histone deacetylase, decreases in diabetic rat kidney and this decrease is overcome by IF. Moreover, we provide evidence for involvement of mitogen activated protein kinases (MAPK) cascade in mediating the effects of IF as there is reduction in the expression of p38 which gets induced under diabetic condition. This was further accompanied by the concomitant decrease in cleavage of caspase3 and p53 expression. These findings suggest that IF significantly improves biochemical parameters associated with development of DN and changes the expression of Sir2 and p53.
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PMID:Intermittent fasting prevents the progression of type I diabetic nephropathy in rats and changes the expression of Sir2 and p53. 1731 25

Curcumin (U1) has a wide spectrum of therapeutic effects such as antitumor and anti-inflammatory effects, including antibacterial, antiviral, antifungal, and antispasmodic activities. By comparison of the structure-activity relationship, tetrahydrocurcumin (THU1), one of the major metabolites, showed the highest antioxidative activity in both in vitro and in vivo systems. U1 has been reported to have the nephroprotective effect to improve creatinine and urea clearance and also protected the chronic renal allograft nephropathy. These beneficial effects have been explained by the protection of oxidative stress and the induction of antioxidative enzymes. The protective effect of THU1 against ferric nitrilotriacetate (Fe-NTA)-induced oxidative renal damage using male ddY mice was greater than that of U1, by monitoring not only radical scavenging activity measured by ESR, and TBARS, 4-HNE-modified protein and 8-OHdG formation but also induction of anioxidative enzymes and detoxification enzymes. THU1 was also expected to improve redox regulation through glutathione and suppress the oxidative stress in diabetic nephropathy and neuropathy. Earlier studies reported that U1 reduced the iron-induced hepatic damage, aflatoxin- and benzo[a]pyrene- induced mutagenicity and hepatocarcinogenecity and also the formation of the DNA adduct by inhibiting cytochrome P450 in the liver. The hepatoprotective role of U1 has been examined using carbone terachloride-induced liver damage in rats and alcoholic liver disease model rats, but not examined using THU1. Our recent data suggests that THU1 is a more promising hepatprotective agent because of its strong induction activity of antioxidant and phase 2-metabolizing enzymes in liver compared to kidney, although more detaied examinations are required.
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PMID:Nephroprotective and hepatoprotective effects of curcuminoids. 1756 22

Transforming growth factor (TGF)-beta plays a critical role in diabetic nephropathy. To isolate the contribution of one of the signaling pathways of TGF-beta, the Smad3 gene in the mouse was knocked out at exons 2 and 3, and the effect was studied in streptozotocin (STZ)-induced diabetes over a period of 6 wk. TGF-beta activity was increased in the diabetic mice but was not able to signal via Smad3 in the knockout (KO) mice. As expected in the wild type, the kidneys of the STZ-diabetic mice showed both structural and functional defects that are characteristic of diabetic renal involvement. In the Smad3-KO mice, however, the defects that were improved were renal hypertrophy, mesangial matrix expansion, fibronectin overproduction, glomerular basement membrane thickening, plasma creatinine, and the blood urea nitrogen. The parameters not significantly altered by the Smad3-KO were albuminuria, reduction in podocyte slit pore density, and the increase in vascular endothelial growth factor abundance and activity. It seems that the absence of Smad3 modifies the natural course of murine diabetic nephropathy, providing renal functional protection and preventing structural lesions relating to kidney hypertrophy and matrix accumulation, even though albuminuria and changes in podocyte morphology persist. In conclusion, the effects of the Smad3-KO mirror the effects of anti-TGF-beta therapy in diabetes, suggesting that the chief component of TGF-beta signaling that is relevant to kidney disease is the Smad3 pathway.
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PMID:Interference with TGF-beta signaling by Smad3-knockout in mice limits diabetic glomerulosclerosis without affecting albuminuria. 1780 83

Type-2 diabetes mellitus (T2DM) is a global disease and its resultant complication, diabetic nephropathy, is a leading cause of chronic renal failure. Microalbuminuria is an early indicator of diabetic nephropathy and is also an independent risk factor for cardiovascular morbidity. Data have shown that anti-hypertensives like Angiotensin receptor blockers (ARB), and Angiotensin converting enzyme inhibitors (ACEI) reduce microalbuminuria and retards the progression of renal disease effectively in hypertensive T2DM patients. But the effects ofARBs on preventing microalbuminuria and ensuing nephropathy in normotensive patients with T2DM is yet to be fully established. To assess the anti-microalbuminuric effects of losartan therapy in normotensive T2DM patients. Interventional Phase Two Clinical Trial was done. Study was done at Diabetic Clinic, Jinnah Hospital Lahore, Pakistan over 8 months. A total of 171 normotensive patients with T2DM and microalbuminuria were evaluated. After informed consent and baseline 24-hour urinary microalbuminuria quantification the selected patients were started on losartan 50 mg/day for a six-month period. Monthly follow-ups were done to monitor the blood pressure, glycemic control, urea/creatinine/potassium levels and any untoward effects of losartan therapy. Quantitative microalbuminuria was repeated at the end of study. Out of the 171 patients, 149 (87.1%) had significant albuminuria reduction >30.0% of their baseline and the variable of final outcome of intervention (urinary albumin in mg/dl) was significantly reduced (Mean 101.9 +/- SD 21.7 baseline and 47.5 +/- 12.9 post therapy) with p<0.001 and with minimal side-effects. These anti-albuminuric effects of losartan were reversible as seen on rechecking the urinary albumin two months after discontinuation of treatment. Losartan was well tolerated and demonstrated significant anti-proteinuric effects in patients with T2DM with early nephropathy independent of hypertension, warranting further long-term large-scale studies to prove its usefulness as preventive therapy for diabetic nephropathy.
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PMID:Use of losartan in reducing microalbuminuria in normotensive patients with type-2 diabetes mellitus. 1789 53

Diagnosis of diabetic nephropathy in the early stages is very important since there are no clinical signs or symptoms. Urinary N-acetyl-beta-D-glucosaminidase (NAG) excretion has been recommended as a tubular dysfunction marker that elevates before other markers, such as microalbuminuria and a decrease in creatinine clearance. In this study, we compared excretion of urinary enzymes with other markers that are used routinely in diabetic nephropathy assessment. Urinary NAG, lactate dehydrogenase (LDH), alkaline phosphatase (AP) activities, urea, creatinine, and albumin, with levels of serum glucose and creatinine and whole blood glycosylated hemoglobin (HbA1c) were measured in 32 diabetes mellitus patients and 25 healthy subjects (controls). Notably, urinary NAG, AP, LDH excretion, and microalbuminuria in the diabetic patients group were significantly increased compared to those in the control groups (P<0.001, P<0.05, P<0.01, and P<0.01, respectively). Meanwhile, our results showed that the urinary NAG excretion had the highest sensitivity and specificity (100% and 87.5%, respectively) compared to other markers. We showed that measuring urinary NAG excretion could be useful for the assessment of renal failure in diabetes mellitus patients and confirmed the use of NAG as a routine screening test.
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PMID:Determination of urinary enzymes as a marker of early renal damage in diabetic patients. 1802 29

The therapeutic potential of lipoic acid (LA) in diabetes and diabetic nephropathy treatment was elucidated. Alloxan diabetic rabbits were treated daily for three weeks with either 10 or 50 mg of LA per kg body weight (i.p.). The following parameters were measured: 1) serum glucose, urea, creatinine and hydroxyl free radical (HFR) levels; 2) blood glutathione redox state; 3) urine albumin concentration; 4) hepatic and renal HFR levels, GSH/GSSG ratios, cysteine contents and the activities of the enzymes of glutathione metabolism; and 5) the activity of renal NADPH oxidase. Histological studies of kidneys were also performed. The treatment of diabetic rabbits with 50 mg of LA resulted in lethal hypoglycaemia in 50% of animals studied. Although the low dose of LA did not change serum glucose concentration, it decreased serum urea and creatinine concentrations, attenuated diabetes-induced decline in GSH/GSSG ratio and abolished hydroxyl free radicals accumulation in serum, liver and kidney cortex. LA did not change the activities of the enzymes of glutathione metabolism, but it elevated hepatic content of cysteine, which limits the rate of glutathione biosynthesis. Moreover, LA lowered urine albumin concentration and attenuated glomerulopathy characteristic of diabetes. However, it did not affect diabetes-stimulated activity of renal NADPH oxidase. In view of these data, it is concluded that low doses of LA might be useful for the therapy of diabetes and diabetic nephropathy. Beneficial action of LA seems to result mainly from direct scavenging of HFR and restoring glutathione redox state due to elevation of intracellular cysteine levels.
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PMID:Lipoic acid ameliorates oxidative stress and renal injury in alloxan diabetic rabbits. 1815 51

It has been documented that green tea (GT) and its catechin components improve renal failure and inhibit the growth of mesangial cells. In the present study we examined the long-term effect of GT extract on streptozotocin (STZ)-induced diabetic nephropathy and on the glycogen accumulation in the kidney tubules. Male Sprague-Dawley rats were randomly assigned to normal control groups (2, 6, 8 and 12 weeks) and five diabetic groups (n 10) of comparable age. A GT diabetic group received 16 % concentration of GT for 12 weeks post-diabetes induction as their sole source of drinking water. GT treatment significantly (P < 0.01) reduced the serum glucose, glycosylated protein, serum creatinine and blood urea N levels by 29.6 (sem 3.7), 22.7 (sem 5.2), 38.9 (sem 10) and 41.7 (sem 1.9) %, respectively, compared with the diabetic group of comparable age. In addition, the GT-treated group showed a significant 44 (sem 10.8) % higher creatinine clearance (Ccr) compared with the untreated diabetic group. Likewise, GT reduced the urea N, creatinine, glucose and protein excretion rates by 30 (sem 7.6), 35.4 (sem 5.3), 34.0 (sem 5.3) and 46.0 (sem 13.0) % compared with the 12 weeks diabetic group. Administration of GT to 12 weeks diabetic rats significantly (P < 0.001) prevented (99.98 (sem 0.27) % less) the accumulation of glycogen in the kidney tubules. These results indicate that in STZ diabetes, kidney function appears to be improved with GT consumption which also prevents glycogen accumulation in the renal tubules, probably by lowering blood levels of glucose. Therefore, GT could be beneficial additional therapy in the management of diabetic nephropathy.
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PMID:Effect of green tea on kidney tubules of diabetic rats. 1825 21

To document clinical, serum and urinary parameters in patients with features of diabetic nephropathy in type 2 diabetes mellitus and to correlate light microscopical findings of the renal biopsy specimen with the clinical, serum and urinary parameters, a study was conducted among 30 patients of type 2 diabetes mellitus with features of nephropathy attended Medical College, Kolkata with special emphasis given on neurological and fundoscopic examination. The patients were investigated with fasting and postprandial venous plasma glucose, glycosylated haemoglobin (HbA1c), serum urea, creatinine, sodium, potassium, 24-hour urinary protein/micro-albumin and lipid profile. Percutaneous renal biopsy was performed after taking informed consent from the patients and sent for histopathological examination. Obtained data were tabulated and analysed. Among 30 patients (male-16; female-14; proteinuric-23, micro-albuminuric-6) diabetic nephropathy was detected in 28 patients (diffuse-15, nodular-9, 4 had focal segmental glomerulosclerosis) and 2 had normal renal biopsy. Retinopathy was detected in 16 patients; 12 had autonomic neuropathy and 3 had peripheral neuropathy.
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PMID:A study on nephropathy in type 2 diabetes mellitus: histology and its correlation with clinical and biochemical parameters. 1838 54

Resveratrol has been reported to have a wide variety of biological effects. However, little is known regarding its role on phosphorylation of histone H3, MAP kinase p38, SIR2 and p53 in type I diabetic nephropathy (DN). Hence, the present study was undertaken to examine changes in the above said parameters by resveratrol treatment. Male Sprague-Dawley rats were rendered diabetic using a single dose of streptozotocin (55 mg/kg, i.p.). DN was assessed by measurements of blood urea nitrogen and creatinine levels. Phosphorylation of histone H3, SIR2, p53 and MAP kinase p38 expression were examined by western blotting. This study reports that treatment of resveratrol prevents the decrease in the expression of SIR2 in diabetic kidney. It also prevents increase in p38, p53 expression and dephosphorylation of histone H3 in diabetic kidney. This is the first report which suggests that protection against development of diabetic nephropathy by resveratrol treatment involves change in phosphorylation of histone H3, expression of Sir-2, p53 and p38 in diabetic kidney.
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PMID:Change in histone H3 phosphorylation, MAP kinase p38, SIR 2 and p53 expression by resveratrol in preventing streptozotocin induced type I diabetic nephropathy. 1840 39


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