Parenchymal nephropathy

Most progressive nephropathies share a final common pathway to irreversible renal parenchymal damage and ESRD (Fig. 76-1). Key pathway elements are loss of nephron mass, glomerular capillary hypertension, and proteinuria. 

The terminology used to describe conditions associated with prominent renal calcium deposits dismisses the importance of the phosphate anion. Renal parenchymal injury with prominent calcium oxalate deposition is referred to as oxalate nephropathy. Oxalate nephropathy is seen in the setting of primary hyperoxaluria or enteric hyperoxaluria secondary to fat malabsorption. Renal parenchymal injury with abundant calcium phosphate deposits is referred to as... 

Seldom are renal parenchymal abnormalities consistent with RPD picked up as an incidental finding on a US, CT or MRl study performed because of a different query, such as interstitial (septic) renal involvement and parainfectious GN in a septic patient, or RPD in a dystrophic child. Contrast-enhanced CT studies may demonstrate delayed and prolonged parenchymal enhancement with reduced cortico-medullary differentiation of enlarged kidneys in acute GN. In general radiopaque intravenous contrast as administered for IVU or CT should be avoided in RPD with renal functional impairment if these studies are performed, good hydration as well as diuretic measures are compulsory to prevent possible contrast nephropathy with renal damage such as papillary necrosis or even renal failure (Erley and Bader 2000 Morcos 1998 Murphy et al. 2000). 

Fig. 19.7a,b. Renal sonography in sickle cell disease, a Increased echogenicity of the medulla with consecutively inverted corticomedullary differentiation. In the absence of hypercalciuria, this pattern is typical for sickle cell nephropathy. b Amplitude-coded color Doppler sonography of the right kidney (cross section) shows a segmental parenchymal area without colour signals (arrow), consistent with a renal infarction in sickle cell disease... 

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