Systemic Sarcoidosis Presenting with Renal Involvement Caused by Various Sarcoidosis-associated Pathophysiological Conditions.

A 61-year-old man was diagnosed with sarcoidosis involving the lungs, eyes, parotid gland and extrathoracic lymph nodes complicated by chronic kidney injury and hypercalcemia. Kidney biopsy showed non-specific interstitial nephritis and nephrosclerosis. However, immunohistochemical staining of cell surface markers revealed a multinucleated giant macrophage surrounded by T-cells, suggesting granulomatous interstitial nephritis. Corticosteroid improved the kidney function, and reduced the serum levels of calcium and angiotensin-converting enzyme. Sarcoid nephropathy may be caused by the combination of several sarcoidosis-associated pathophysiological conditions and a comprehensive kidney examination should be performed to assess the type of injury when determining a treatment strategy.

Hyperuricemia as a Predictive Marker for Progression of Nephrosclerosis: Clinical Assessment of Prognostic Factors in Biopsy-Proven Arterial/Arteriolar Nephrosclerosis.

AIM: The influence of serum urate on kidney disease is attracting attention, but the effects of uric acid (UA) on nephrosclerosis have not been elucidated. METHODS: We reviewed data from 45 patients diagnosed with arterial/arteriolar nephrosclerosis. The renal outcomes of the arterial/arteriolar nephrosclerosis patients were assessed by performing logistic and Cox regression analyses. A Kaplan-Meier analysis was used to evaluate the impact of hyperuricemia (HU) on kidney survival. The renal outcomes of patients with and without HU were compared by using a propensity score-matched cohort. RESULTS: The logistic regression models showed no significant differences in renal outcomes, according to baseline parameters or follow-up parameters, except the serum UA value and body mass index (BMI). Baseline serum UA level had the highest odds ratio (OR) for estimated glomerular filtration rate (eGFR) decline (OR, 1.86; 95% confidence interval (CI), 1.12 to 3.45), among the parameters assessed. In the multivariate Cox regression analysis, HU (UA ≥8.0 mg/dL) (P=0.01) and BMI (P=0.03) were significantly associated with a ≥50% eGFR decline or ESRD. The Kaplan-Meier analysis in the propensity score-matched cohort indicated that the renal survival rate of the group of arterial/arteriolar nephrosclerosis patients with HU was significantly lower than that of the group without HU (log rank, P=0.03). CONCLUSION: The results of this study suggest that the baseline serum UA value can serve as a renal outcome predictor in arterial/arteriolar nephrosclerosis patients.

Renal histology in patients with elevated serum creatinine and concurrent normal urinalysis.

INTRODUCTION: Diagnosis of kidney disease is currently and primarily based on the measurement of serum creatinine, blood urea nitrogen, and urine output, and most kidney diseases with elevated serum creatinine accompany abnormal findings of urinalysis with microscopy, such as proteinuria or hematuria. The purpose of the current study was to determine the histologic diagnosis of patients with elevated serum creatinine and a concurrent normal urinalysis without underlying disease. METHODS: The medical records of patients who had undergone kidney biopsies between January 1, 2003 and March 1, 2008 in three medical centers were retrospectively reviewed. The patients with an elevated serum creatinine level and a normal urinalysis were enrolled. The exclusion criteria were as follows: diabetes mellitus; hypertension; chronic liver disease; malignancies; autoimmune diseases; dependence on medications; hypokalemic nephropathy; age < 18 years. Age, duration of follow-up, post-biopsy management, and the change in levels of BUN and serum creatinine from pre-biopsy to the last visit were analyzed. RESULTS: All 15 patients were included. The most frequent single diagnosis was acute interstitial interstitial nephritis, followed by hypertensive nephrosclerosis. Chronic interstitial nephritis, mesangial proliferative glomerulonephritis, acute tubular necrosis, secondary amyoloidosis, focal segmental glomerulosclerosis, and minor glomerular change were listed. The young group (< 40 years of age) included more patients with acute interstitial nephritis, and the old group (≥ 40 years of age) included more patients with hypertensive nephrosclerosis. CONCLUSION: Based on a correct histological diagnosis, all of the patients, except one, were properly managed and had preserved kidney function until the last visit.

[Early diagnosis of nephrosclerosis in children with vesicoureteral reflux].

Comparison of results of standard complex of survey with changes of urine levels of biological inflammatory marker (MCP-1), marker of fibrogenesis (TGF-beta1), marker of angiogenesis (VEGF), markers of nephron damage (collagen IV, alpha-GST, pi-GST) in 140 children with vesicoureteral reflux before and 6 months after treatment was performed. It was found that nephrosclerotic process occurs even at low degrees of vesicoureteral reflux. Even in the absence of structural and functional disorders of the kidneys according to traditional methods of evaluation, there were significant changes in the levels of biological markers of inflammation, fibrosis, and angiogenesis, as well as damage of main elements of the nephron. The method for calculating the "index of early renal damage" is proposed; method allows to monitor the state of the renal parenchyma of children with this disease.

"Benign" hypertensive nephrosclerosis.

BACKGROUND: Whether benign hypertensive nephrosclerosis (BHN) causes end-stage renal failure (ESRF) is controversial. One reason for this is the lack of biopsy evidence confirming the clinical diagnosis in most cases. AIM: To investigate whether biopsy-proven BHN leads to ESRF. DESIGN: Retrospective analysis. METHODS: We analysed all cases of biopsy-proven BHN from a single centre over a period of 20 years (n = 60), followed-up for a mean +/- SD 6.7 +/- 5.5 years. RESULTS: Patients were divided into those with stable renal function (n = 17) and those with declining function (n = 43). Mean eGFR at the time of biopsy was lower in the declining function group (29 +/- 3 vs. 44 +/- 4 ml/min/1.73 m(2), serum creatinine 280 +/- 165 vs. 161 +/- 89 mumol/l, p < 0.001), of whom 72% progressed to ESRF. Median renal survival for the whole group was 6.8 years, with 5- and 10-year survivals of 56% and 35%, respectively. Renal survival was significantly affected by initial serum creatinine, and mean systolic and diastolic blood pressures during follow-up period. Mean protein excretion was higher in the declining group, but not significantly so. On multivariate analysis, only diastolic blood pressure during follow-up predicted renal survival (p = 0.017). Median patient survival for the whole group was 9.95 years post renal biopsy, with 5- and 10-year survivals of 70% and 49% respectively. Survival was affected by initial serum creatinine, initial serum albumin and mean systolic blood pressure during follow-up. On multivariate analysis, only initial serum creatinine was significantly correlated with survival (p = 0.017). DISCUSSION: Biopsy-proven BHN led to ESRF in a high percentage of our patients, and was associated with significant mortality.

Possible relationship between hyperinsulinemia and glomerular hypertrophy in nephrosclerosis.

Hyperinsulinemia is potentially associated with the development of vascular sclerosis. On the other hand, the relationship between hyperinsulinemia and nephrosclerosis has not been elucidated. In this investigation clinicopathological studies were performed in 40 patients with nephrosclerosis, with special attention to the relationship between hyperinsulinemia and glomerular hypertrophy. Forty patients with biopsy-proven nephrosclerosis were divided into two groups by the 75-g oral glucose tolerance test (OGTT): group A, 2-hr plasma glucose concentration > 140 mg/dL (n = 25); group B, 140 < or = 2-hr plasma glucose < 200 mg/dL (n = 15). Patients with diabetes mellitus or diabetic nephropathy were not included. Morphometric analysis of the glomeruli revealed a significantly larger mean glomerular volume in subjects with nephrosclerosis in both subgroups. In addition, the mean glomerular volume was significantly correlated with the fasting insulin level, while no significant correlation was observed between the mean glomerular volume and creatinine clearance or degree of global sclerosis. These results indicate that hyperinsulinemia may be intimately related to glomerular hypertrophy in patients with nephrosclerosis.

Sodium balance and plasma renin activity during the development of two-kidney Goldblatt hypertension in rats.

1. In two experiments severe hypertension (systolic blood pressure 180 mmHg) was induced in rats by constricting one renal artery with a silver clip (two-kidney, one clip hypertension; 2KIC). Blood pressure, plasma renin activity (PRA) and body weight were measured for 35 days after clipping. Plasma sodium concentration and carcass sodium content were measured at the conclusion of the experiment. To determine the relationship between sodium intake, PRA and the development of severe hypertension, half of the rats were given a normal diet and water to drink; the other half were given a low sodium diet and 0.9% saline to drink. 2. In both experiments, two patterns of responses were observed. Group (1) had reduced growth rate, and marked elevation of PRA. Some, but not all of these animals had histological evidence of malignant nephrosclerosis in the untouched kidney. In the other group (11), weight gain was normal and PRA was normal or only slightly elevated. 3. Group 1 animals drinking saline, had raised carcass sodium levels, whereas those drinking water had no increase in carcass sodium. 4. The results confirm that hypertension in the 2KIC model is not always associated with a raised PRA. 5. The coexistence of a raised PRA and increased total body sodium suggests that the PRA does not rise as a result of sodium depletion in this model.