A concurrence of light and heavy chain deposition disease and diabetic nephropathy.

A 56-year-old female patient was clinically characterized by heavy proteinuria, anemia, hypertension, and no detectable monoclonal protein in serum or urine. She had a history of diabetes with retinopathy and hypertension. Histological investigation of renal biopsy specimens revealed nodular glomerulosclerosis. Light microscopic examination did not allow discrimination between diabetic glomerulosclerosis and monoclonal immunoglobulin deposition disease (MIDD). Immunofluorescent examination showed linear capillary wall and tubular basement membrane staining with kappa, and IgG staining. Electron-microscopic examination confirmed the amorphous material along the glomerular basement. Based on these findings, the diagnosis of light chain and heavy chain monoclonal immunoglobulin deposition disease (LHCDD) and diabetic nephropathy was made. At the present after the 7th course of melphalan and prednisolone treatment, her renal function and proteinuria have progressively improved.

Therapeutic dose of acetaminophen with fatal hepatic necrosis and acute renal failure.

A 33-year-old woman without evidence of previous liver disease developed fulminant hepatic failure following the therapeutic dose of acetaminophen 3 days prior to admission. At admission, liver and renal function revealed hepatocellular injury with jaundice, and acute renal failure, total serum bilirubin 12.5 mg/ dL, direct serum bilirubin 8.1 mg/dL, aspartate aminotransferase 8460 IU/L, alanine aminotransferase 4640 IU/L, blood urea nitrogen 36 mg/dL, and serum creatinine 5.2 mg/dL. Two days later she developed multiorgan failure including hemodynamic disturbance with irreversible shock, and expired. Autopsy was performed, liver pathology showed severe centrilobular and midzonal necrosis, compatible with toxic hepatic necrosis, and renal pathology showed focal loss of tubular epithelial cells and partial occlusion of tubular lumen by cellular debris, compatible with acute tubular necrosis. Physicians should be aware of potential hepatotoxicity and nephrotoxicity of acetaminophen, even if given at therapeutic dosage in acute febrile illness.

Predictors of renal involvement in patients with systemic lupus erythematosus.

From a cohort of 109 patients (105 females and 4 males) treated for systemic lupus erythematosus (SLE), 20 patients (18.3%) developed new episodes of lupus nephritis and 89 patients (81.7%) remained free of renal involvement during the follow-up period. The mean duration of follow up was 39.1 +/- 54.4 months. Clinical characteristics associated with developing lupus nephritis were a high systolic blood pressure (> or = 130 mmHg), photosensitivity, cutaneous vasculitis and gastrointestinal (GI) symptoms. Laboratory abnormalities associated with the development of lupus nephritis were hemoglobin < 10 mg/dl, hematocrit < 30%, blood urea nitrogen > 12 mg/dl, serum creatinine > 1.3 mg/dl, ESR > 60, the third component of complement (C3) level < 0.45 and positive antidsDNA antibody. After a multivariable analysis, only high systolic blood pressure, cutaneous vasculitis, hemoglobin < 10 mg/dl and serum creatinine > 1.3 mg/dl remained as statistically significant risk factors for developing lupus nephritis.

Estimating glomerular filtration rate in Asian patients with chronic kidney diseases from bioelectrical impedance analysis.

BACKGROUND: Estimation of glomerular filtration rate (GFR) is usually determined from 24-hour urine collection, but it is time-consuming, and difficult in clinical practice. The authors attempted to select an accurate and safe, but more convenient test to obtain an estimated GFR. Objective: To compare estimation of GFR by Bioelectrical impedance analysis (BIA) with GFR calculated by 24-hour urine averaged creatinine clearance and urea clearance (Ccr-Cu-GFR). MATERIAL AND METHOD: The authors examined 79 non-diabetic chronic kidney disease (CKD) patients that had estimated GFR between 15 and 89 ml/min/1. 73 m(2). Subjects were categorized into three subgroups according to K/DOQI-CKD classification: GFR of 60-89 m/min/1. 73m(2) (stage 2, 5 subjects), 30-59 ml/min/ 1.73m(2) (stage 3, 31 subjects), and 15-29 ml/min/1.73m(2) (stage 4, 43 subjects). RESULTS: The mean value of Ccr-Cu-GFR was 33.79+/-14.78 ml/min/1. 73 m(2) and GFR by BIA (BIA-GFR), 34.63 +/- 14.86 ml/min/1. 73 m(2) with no overall statistical differences (p = 0.838). In stage 3 CKD patients, the mean BIA-GFR and Ccr-Cu-GFR were similar (38.84+/-12.47 vs 41.16+/-9.17, p = 0. 399) while in stage 2 CKD, BIA-GFR tended to underestimate (63.50+/- 19.35 vs 70.94+/-7.82, p = 0.407) and in stage 4 CKD, BIA-GFR significantly overestimated Ccr-Cu-GFR (27.31+/-9.11 vs 23.76+/-5.68, p = 0.040). CONCLUSION: The findings suggest that BIA-GFR in non-diabetic CKD patients closely resembled with Ccr-Cu-GFR especially in stage 3 CKD patients. BIA-GFR may be considered as a more convenient test for an assessment of GFR in non-diabetic CKD patients.

The correlation of insulin resistance and renal function in non diabetic chronic kidney disease patients.

INTRODUCTION: A greater degree of insulin resistance may predispose to renal injury by worsening renal hemodynamics through the elevation of glomerular filtration fraction. However, there are sparse data on the relationship between insulin resistance, glomerular filtration rate (GFR) and body composition in chronic kidney disease (CKD) without diabetes. OBJECTIVES: To evaluate the relationship between insulin resistance, total body fat and GFR in CKD without diabetes. MATERIAL AND METHOD: The authors screened 84 non-diabetic CKD patients according to the K/DOQI definitions and only 78 patients were enrolled into the study (CKD stages 2-4, GFR between 15 and 90 ml/min/ 1.73 m2). Insulin resistance was evaluated by homeostasis model assessment (HOMA-IR). Bioelectrical impedance analysis was performed to determine the percentage of total body fat. GFR was calculated by the average of creatinine and urea clearances. RESULTS: The correlation analysis showed that HOMA-IR was positively correlated with percent body fat (r = 0.32, P<0.05), BMI (r = 0.46, P<0.01), serum triglyceride (TG) (r =0.29, P<0.01), and mean arterial pressure (r =0.25, P<0.05), but not significantly correlated with GFR, age, cholesterol, HDL, uric acid and 24-hr urinary protein. CONCLUSION: In non-diabetic CKD patients, the independent factor for insulin resistance was the amount of total body fat. The insulin level and HOMA-IR were not dependent on the GFR in the present study.