Green tea and bilberry protective effect against gentamicin-induced nephrotoxicity in rats

The aim of our study was to investigate if green tea and bilberry have protective effect on gentamicin-induced kidney damage, when applied together, and to make a connection between their effects. GM group of rats received only gentamicin, GT group received green tea only, B group received only bilberry, whereas control (C) group received saline only. GT+GM group received green tea together with gentamicin, and B+GM group received bilberry together with gentamicin. Biochemical analysis showed significantly increased urea and creatinine levels in GM group when compared to groups that also received bilberry or green tea. Histological analysis showed complete disruption of glomerular basal membrane as well as basal membranes of both proximal and distal tubules in GM group. These destructive effects were significantly milder and limited only to proximal tubules when bilberry or green tea was applied simultaneously with gentamicin. Both green tea and bilberry protective effect on gentamicin-induced nephrotoxicity is manifested because of their strong antioxidant activity. Since they are strong antioxidants, widely distributed in nature, they can offer available and inexpensive adjuvant therapy in Gram-negative infections, which can relieve gentamicin nephrotoxicity, but will not affect its bactericidal effect.

Histopathology Interstitial Severity Index Associated with Glomerular and Tubular Severity Index in Nephrotic Syndrome Patients

Introduction: Nephrotic syndrome is characterized by massive proteinuria due to leakage of glomerular basal membrane, and subsequent process in tubular and interstitial tissue. It should be elucidated whether the severity of histopathological lesions in compartments of kidney tissue play a role and whether lesion in those compartments associated one to another. Aim: The study aims to correlate severity histopathologic lesions among compartments in kidney tissue. Method: All patients with nephrotic syndrome were biopsied and the cores were stained with Hematoxylin-Eosin, PAS, Masson’s Trichrome to look at glomerular, tubular, interstitial and vascular involvements. Glomerular abnormalities including mesangial hypercellularity, endocapillary hypercellularity, membranous; tubular, interstitial, and vascular severities were scored according to type, activity, severity and distribution in histopathologic features. Results: This study included 46 patients consisted of 16 (34.8%) males and 30 (65.2%) females, aged 26 ± 10 years, SBP 121.7 ± 13.10 and DBP 78.21 ± 7.80 mmHg, diagnosed with 14 lupus and 32 non-lupus nephrotic syndrome. Histopathologic abnormalities showed glomerular index was 4.26 ± 2.34, tubular index was 3.09 ± 1.90, interstitial index was 3.02 ± 1.48, vascular index was 0-3, pathologic index was 10.56 ± 4.54. There was significant correlation of severity index between interstitial and glomerular lesions (R=0.49, P=0.001), and between interstitial and tubular lesions (R=0.45, P=0.002). However, there were no significant correlations of severity index between interstitial and vascular lesions, and glomerular and tubular lesions. Conclusion: There are significant correlations of severity index between interstitial with glomerular and tubular lesions. It may implicate that histopathological process in interstitial tissue plays a central role in the pathogenesis of proteinuria in nephrotic syndrome.

Proteinuria inducing tubulointerstitial damage

Introduction Glomerular basal membrane represents a mechanical and electric barrier for plasma proteins. In physiological conditions only plasma proteins of low molecular weight are completely filtered through basal membrane. Due to damages of glomerular basal membrane there is an increase in filtration of plasma proteins of moderate and high molecular weight. Proteinuria In regard to its etiology proteinuria can be prerenal, renal and postrenal. By analyzing albumin, 1-microglobulin, immunoglobulin G and 2-macroglobulin, together with total protein in urine, it is possible to detect and differentiate causes of prerenal, glomerular, tubular and postrenal proteinuria. Abnormal glomerular permeability to macromolecules results in excessive protein delivery and reabsorption in proximal tubules. Excessive reabsorption in turn may cause congestion of intracellular endocytic and biosynthetic compartments leading to NFkB-dependent and -independent gene upregulation. Among those genes, monocyte chemoattractant protein-1 (MCP-1), cytokines, osteopontin and endothelin stimulate processes of interstitial inflammation and fibroblast proliferation and are ultimately responsible for enhanced extracellular matrix deposition and renal scarring. Human tubular cells exposed to albumin and HDL increase production of endothelin-1. Endothelin-1 affects microcirculation and fibroblasts and is a monocyte chemoattractant. Specific proteins that are cytotoxic are transferrin/iron, low-density lipoprotein, and complement components, all of which appear in urine in proteinuric states. Adequate and early diagnosis and differentiation of proteinuria are of immense therapeutic importance.

Glycosaminoglycans in therapy of diabetic nephropathy

Sulodexide, a drug containing glycosaminoglycans, was used in the treatment of patients with type I diabetes. Along with their effects on the blood clotting system, glycosaminoglycans are capable of preventing the mesangial proliferation and hyperproduction of extracellular matrix, as well as thickening of the glomerular basal membrane and impairment of its permeability and charge selection. A reliable antiproteinuric effect of the drug was noted, persisting for 6 weeks after it was discontinued; the excretion of protein with the urine reliably decreased in patients with both, microalbuminuria and proteinuria. Moreover, an antiatherogenic effect (a reliable decrease of serum atherogenicity coefficient) of sulodexide was observed. Assessment of the status of the fundus oculi of diabetics treated with sulodexide demonstrated a positive dynamics during therapy in some of the patients with nonproliferative and preproliferative retinopathy; no deterioration as regards the fundus oculi were noted. Hence, addition of sulodexide to combined therapy of patients with diabetic nephropathy is effective and pathogenetically justified.