The determination of insulin sensitivity in hemodialysis and continuous ambulatory peritoneal dialysis in nondiabetic patients with end-stage renal disease.

OBJECTIVE: To determine the beta-cell function and insulin sensitivity with homeostasis model assessment (HOMA) and area under curve (AUC) in nondiabetic uremic hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) patients cross sectionally. METHODS: The study was performed between January to August 2001 in the Department of Nephrology, Dicle University School of Medicine, Diyarbakir, Turkey. Fifty-one HD patients, 45 CAPD patients, and 50 healthy control subjects were included in the study. Height, weight, waist and hip circumference, fat mass and percentage of body fat, and body mass index (BMI) were measured. The total high density lipoprotein (HDL) and low density lipoprotein (LDL)-cholesterol, triglyceride, urea, creatinine, insulin, potassium, parathyroid hormone (PTH) and 1,25 dihydroxycholecalciferol levels were measured. Oral glucose tolerance test (OGTT) was performed in the mid-week dialysis-free interval in HD patients, whereas after at least a night without dialysis exchanges in CAPD group. Area under curve both of insulin and glucose were calculated. The HOMA [insulin sensitivity (%S)] and AUC were used as indices of tissue insulin sensitivity. RESULTS: The LDL-cholesterol levels of patients with CAPD was higher than the HD group (p<0.001) and control group (p<0.0001). The baseline glucose levels of the 2 groups were not significantly different. Baseline insulin levels of CAPD group were higher than the HD group (p<0.001) and the control group (p<0.0001). Area under curve for glucose (AUCgluc) and insulin (AUCins) value of CAPD patients were higher than the HD patients than the control group (p<0.0001). The HOMA [beta-cell function (%B)] values of CAPD group were higher than both HD (p<0.02) and control group (p<0.04). The HOMA [insulin sensitivity (%S)] levels of CAPD group was significantly lower than the HD patients (p<0.002) and the control group (p<0.001). CONCLUSION: The CAPD treatment may lead to insulin insensitivity in non-diabetic end-stage renal disease patients and the high glucose content of CAPD solutions may be responsible for insulin resistance in CAPD patients.

Does the analysis based on a histological and immunohistochemical grading system in the model of BDL kidney allow the quantification of the degree of injury?

The aim of this study is to evaluate histopathological findings induced by Nomega-nitro-L-arginine methyl ester (L-NAME) and molsidomine (MOL) on the kidney of bile duct ligated rats. Forty Sprague-Dawley rats, each weighing 125 to 140 g, were included in the study. Extent of histological glomerular injury scores (GIS), arterial injury scores (AIS), and tubulointerstitial injury scores (TIS) in each animal were graded. Alpha-smooth muscle actin (alpha-SMA), tenascin, lectin (Ulex europaeus agglutinin-1), and vimentin were used to determine extent of the injury. The cholestasis was evidenced by a significant increase in the levels of serum total bilirubin in BDL rats (p < 0.01). Malondialdeyde MDA levels increased by the bile duct ligation (BDL) to 12.10 +/- 0.45. This value was significantly higher than the other groups (p < 0.01). Changes in the BDL kidney were marked at 7 days after surgery. GIS were observed to have the highest score, especially at juxtamedullary region in BDL/L-NAME rats, and AIS were also the highest score in this region. These observations were lower in BDL/MOL rats. There is a correlation between GIS and AIS scores (r = .2, p < .01). TIS revealed that BDL/L-NAME rats were significantly more damage than rats in the other groups (p<.001). MOL-treated rats showed considerably fewer lesions in the tubules and interstitium (p < .001). The tubular injuries observed in BDL and BDL/L-NAME rats were significantly attenuated by MOL treatment. Lectin was more and extensively stained in tubular epithelia of the BDL/L-NAME group than in the other (p <.05). Expression of tenascin in tubular epithelia was significantly higher in BDL and BDL/L-NAME as compared with controls (p < .01). Fibrous tissue was only observed in the BDL and BDL/L-NAME group. These areas were weakly stained with vimentin. alpha-SMA staining was more reduced in the L-NAME-treated arterioles than in BDL/MOL (p < .05). In conclusion, the analysis of cell injury based on a histological grading system in the model of BDL kidney allows the quantification of the degree of injury.

Influence of L-NAME and L-Arg on ischaemia-reperfusion induced gastric mucosa damage.

OBJECTIVE: The aim of this study was to investigate effects of L-NAME and L-Arginine on gastric mucosal injury induced by ischaemia-reperfusion. METHODS: In the experiment, 20 New Zealand rabbits were used (2700-3000 g). Celiac artery was clamped for 30 min for ischaemia and then 60 min of reperfusion followed this after all rabbits were anaesthetized. In the Sham-control group (G 1, n = 5), laparotomy was performed, and the celiac artery was prepared without clipping. Group 2 (Untreated, n = 5) rabbits were only subjected to ischaemia-reperfusion. Group 3 (n = 5) rabbits had L-Arginine Methyl Ester (L-Arg) 3 mg/kg/min as i.v. infusion during the first 15 min of the reperfusion. Group 4 (n = 5) rabbits had a nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME) 100 micrograms/kg/min i.v. during the first 15 min of the reperfusion. After 60 min of reperfusion, the rabbits were killed, and their stomachs were removed for histopathologic evaluation and determination of malondialdehyde (MDA) level. RESULTS: After ischaemia-reperfusion, Untreated group had macroscopic necrosis involving 50 +/- 6% of total gastric mucosa area and deep mucosal necrosis involving 10 +/- 5% of mucosal strips. In the group treated with L-NAME, macroscopic mucosal necrosis involved 52 +/- 6% of total gastric mucosa area and deep mucosal necrosis involved 11 +/- 3% of mucosal strips (both p > 0.05 versus Untreated group). L-Arg treatment significantly reduced macroscopic mucosal necrosis area to 20 +/- 6% and deep mucosal necrosis to 3 +/- 1% (both p < 0.05 versus Untreated group and L-NAME group). MDA level in the L-Arg group was significantly lower when compared to control and L-NAME group MDA level (p < 0.05). CONCLUSION: These results suggest that NO increase induced by L-Arginine injection is involved in the protection of gastric mucosa after ischaemia-reperfusion.

Crescentic glomerulonephritis requiring hemodialysis and elevated MPO-ANCA level and vasculitis allergica cutis in a 21-year-old girl.

Microscopic polyangiitis (mPA) is a systemic necrotizing nongranulomatous vasculitis that affects small blood vessels. Clinical features include constitutional symptoms such as fever, anorexia, fatigue, and weight loss. Skin lesions include purpura and splinter hemorrhages, which occur in 50% of patients. Another characteristic feature is rapidly progressive glomerulonephritis, which often affects the kidneys in the early stages of the condition. Diagnosis is based on typical clinical features, biopsy, and presence of antineutrophil cytoplasmic antibodies (ANCA). This disorder tends to involve middle-aged and older persons, with a predilection for males; it is very rare in children. A 21-year-old female patient with mPA who did not respond well to treatment, required hemodialysis, developed vasculitis allergica cutis (VAC) later, and had a relatively short-term survival is reported herein.