Uronephro Flashcards
How can you assess GFR ?
Measurement through plasma clearance of markers (iohexol, exogenous creatinin, radioisotopes) or urinary clearance (iohexol, inulin). Renal scintigraphy. Biomarkers (Crea, Urea, SDMA +/- cystitin C - rather a tubular dysfunction biomarker, limited utility compared to SDMA or Crea)
Contrindications for renal biopsies ?
IRIS stage 4 CKD, primary tubulointerstitial disease, evidence of hydronephrosis, pyelonephritis, hemostatic disorders, and/or renal abscessation. There is little to gain with biopsy results in a pet likely to have either amyloidosis or a hereditary nephropathy given that, to date, there is no evidence that these dogs or cats will respond to immunosuppressive agents
Indications for renal biopsies ?
Current IRIS guidelines suggest that biopsy be considered for pets with persistent substantial proteinuria (UPCR >3.5), in pets where proteinuria is unresponsive to anti-proteinuric therapy, or pets with progressive worsening proteinuria or decline in renal function despite therapy. Biopsy results help determine if immunosuppressive therapy is indicated.
Pathophysiology of amyloidosis ?
Amyloidosis is a heterogeneous group of diseases characterized by extracellular deposition of insoluble fibrillary proteins with a specific beta-pleated sheet conformation.10 Hereditary amyloidosis is caused by mutant genes encoding variant proteins whose structure makes them amyloidogenic. Amyloid proteins may originate from various precursors and their formation may be primary or secondary (reactive).
Secondary amyloidosis is the most common form in dogs and cats, in which renal amyloid fibrils are composed of an N-terminal fragment of the APP, serum amyloid A.
Repartition of amyloid deposition in renal amyloidosis in CSP ? in Abyssian cats ?
Medullary deposition at first contrary to other breeds (English Foxhound, Beagle, …). Other organs are concerned in CSP (spleen, liver, adrenal glands, …)
How can we make a diagnosis of hereditary nephritis ?
Abnormal collagen type IV formation secondary to COL4A3, COL4A4, COL4A5 mutation -> splitting of the basement mb that can be seen with electron microscopy early in life. Light microscopy: membranoproliferative glomerulonephropathy. Immunohisto: abnormal collagen IV pattern (except in Bull Terrier and Dalmatian !).
What increases FGF-23 secretion ?
Increases in plasma phosphate and calcitriol both stimulate FGF-23 secretion, but how cells producing FGF-23 sense and respond to changes in phosphate concentration is not understood at present.
