Abstract
Patients with collapsing glomerulopathy (CG) have marked proteinuria that rapidly progresses to chronic renal failure. In this study, we investigated if the nephropathy produced in a rat model by the injection of serum from CG patients induced alterations in fatty acid (FA) metabolism. Twenty-four female Sprague-Dawley rats were divided into four groups of six rats each: Group I, control rats (C); Group II, rats that received injections of 1 mL of 0.9% NaCl saline solution (SS); Group III, rats injected with 25 mg/mL of serum from healthy subjects (HS); and Group IV, rats injected with 25 mg/mL of serum from CG patients. In all groups, the systolic blood pressure (SBP), proteinuria, creatinine clearance (CC), cholesterol and total FA composition in the kidney and serum were evaluated. The administration of serum from CG patients to rats induced glomerular collapse, proteinuria, reduced CC and elevated SBP (p ≤ 0.01) in comparison with the C, SS and HS rats. The FA composition of the serum of rats that received the CG serum showed an increase in palmitic acid (PA) and a decrease in arachidonic acid (AA) when compared to serum from HS (p ≤ 0.02). In rats receiving the CG serum, there was also a decrease in the AA in the kidney but there was an increase in the PA in the serum and kidney (p ≤ 0.01). These results suggest that the administration of serum from CG patients to rats induces alterations in FA metabolism including changes in PA and in AA, which are precursors for the biosynthesis of the prostaglandins that are involved in the elevation of SBP and in renal injury. These changes may contribute to collapsing glomerulopathy disease.
Highlights
Collapsing glomerulopathy (CG) is a progressive and aggressive form of glomerular disease that was first described by Weiss et al in 1986 [1], in a small group of six patients with nephrotic syndrome.Eight years later, Detwiler et al [2], reported sixteen patients
Regarding the polyunsaturated FAs (PUFAs), the arachidonic acid (AA) and docosahexaenoic acid were significantly decreased in the serum from collapsing glomerulopathy (CG) patients when compared with the serum from healthy subjects (HS) (p = 0.001 and p = 0.01 respectively)
The CT levels in the kidney showed a tendency to increase without reaching a statistically significant change. These results suggest that the serum of CG patients contains circulating permeability factors that contribute to impaired renal hemodynamics, which are reflected in massive proteinuria and increased systolic blood pressure (SBP) [12]
Summary
Collapsing glomerulopathy (CG) is a progressive and aggressive form of glomerular disease that was first described by Weiss et al in 1986 [1], in a small group of six patients with nephrotic syndrome.Eight years later, Detwiler et al [2], reported sixteen patients. Collapsing glomerulopathy (CG) is a progressive and aggressive form of glomerular disease that was first described by Weiss et al in 1986 [1], in a small group of six patients with nephrotic syndrome. A recent investigation showed that the CG that is present in other nosologies has more aggressive characteristics than the rest of the FSGS types [4]. Lipid-laden macrophages of different sizes are present, and there is glomerular capillary collapse. Some studies have described the presence of several circulating factors in the serum from CG patients such as the soluble urokinase plasminogen activator receptor (suPAR), cardiotrophin-like cytokine factor-1 (CLCF-1) and CD40 antibodies that may cause direct damage to podocytes, provoking their separation from the basal capillary membrane, which results in the alteration of the permeability to albumin [6]
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