![]() Similar results were observed in diabetic patients with normoalbuminuria, suggesting that podocyturia increased significantly prior to the onset of albuminuria. These results are consistent with the increased podocyte loss due to glomerular damage caused by diabetes mellitus ( 10). A recent study showed that diabetic adults with albuminuria had an increased urinary NPHS2 : NPHS1 ratio and urinary NPHS2 : creatinine ratio compared with non-diabetic subjects. The analysis of urinary excretion of NPHS1 and NPHS2 has also been used in human medicine to assess the risk of glomerular injury developing or progressing. However, NPHS1 and NPHS2 detection patterns in the urine of dogs with CKD have not yet been described. Likewise, in humans with progressive glomerular disease, the amount of urine NPHS2 was greater than that in healthy individuals ( 33). ![]() In experimental models, induced glomerular lesions promoted an increase in urinary NPHS1 and NPHS2 excretion, but disease progression was marked only by urine NPHS2 detection ( 25). Nephrin mRNA ( NPHS1) and podocin mRNA ( NPHS2) have been used as podocyte markers in urine ( 9, 33). However, possible differences in podocyturia between CKD stages have not been evaluated. Podocyturia was assessed by urinary podocin concentration using an ELISA test or by podocin detection using liquid chromatography–mass spectrometry, and the CKD group was formed by dogs at different stages of the disease. In these studies, dogs with CKD or degenerative mitral valve disease (DMVD) had greater podocyturia than healthy dogs ( 27, 28). Recent studies have evaluated podocin detection in urine sediments of dogs to estimate podocyturia in these patients ( 27, 28). Several glomerular diseases can cause damage to podocytes, including degenerative, infectious, and metabolic diseases ( 12). Podocyturia can occur naturally in humans ( 31) and horses ( 26) however, an increased extent of podocyturia over what may occur naturally is related to glomerular lesions, with proteinuria as one of the main consequences ( 29). These podocyte changes are frequently accompanied by podocyte detachment, podocyturia and podocytopaenia. It is commonly reported in dogs aged over 12 years ( 21) considering that the care of older dogs needs increasingly frequent veterinarian involvement, the number of CKD cases acquires significance in routine clinical care provision.ĭogs suffering from CKD have alterations in the GFB, which include GBM thickening, loss of adhesion between podocytes and the GBM, and podocyte foot process effacement ( 14). Nephrin, encoded by the NPHS1 gene, is a transmembrane protein in the SD, whereas podocin, encoded by the NPHS2 gene, interacts with the cytoplasmic tail of nephrin and participates in the connection between the SD and the cytoskeleton of foot processes ( 20).Ĭhronic kidney disease (CKD) is characterised by irreversible lesions in the renal parenchyma that compromise the structure and function of nephrons ( 16). The GBM and SD serve as barriers to prevent the filtration of plasma macromolecules such as proteins. Foot processes from neighbouring podocytes interdigitate and are connected by a membrane called the slit diaphragm (SD). ![]() The glomerular filtration barrier (GFB) is formed by glomerular endothelial cells, the glomerular basement membrane (GBM), and podocyte foot processes covering the GBM.
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