Glomerulonephritis clinical presentation

Of 63 adults with advanced renal insufficiency, those with biopsy-proven primary proliferative glomerulonephritis and those whose clinical presentation was consistent with glomerulonephritis had significantly greater exposure to organic solvents than patients with a variety of other renal diseases (37). 

Glomerulonephritis is a collection of glomerular diseases mediated by different immunologic pathogenic mechanisms, resulting in varied clinical presentation and therapeutic outcomes. 

This chapter provides an overview of the pathophysiologic mechanisms of glomerular injury and the clinical presentations of glomerulonephritis. The treatment approach for the common forms of glomerulonephritis are also discussed. Although diabetes mellitus and amyloidosis are important secondary causes of glomerular diseases, the scope of this chapter is limited to the primary causes of glomerulonephritis. 

Diuretic resistance may occur simply because excessive sodium intake overrides the ability of the diuretics to eliminate sodium. Other reasons exist for diuretic resistance in this population. Patients with ATN have a reduced number of functioning nephrons on which the diuretic may exert its action. Other clinical states like glomerulonephritis are associated with heavy proteinuria. Intraluminal loop diuretics cannot exert their effect in the loop of Henle because they are extensively bound to the protein present in the urine. Still other patients may have reduced bioavailability of oral furosemide. Possible therapeutic options to counteract each form of diuretic resistance are presented in Table 42-7. Combination therapy of loop diuretics plus a diuretic from a different pharmacologic class can be an effective tool in the setting of ARF. Loop diuretics increase the delivery of sodium chloride to the distal convoluted tubule and collecting duct. With time, these areas of the nephron compensate for the activity of the loop diuretic and increase sodium and chloride resorption. Diuretics that work at the... 

NSAID induced nephrotic syndrome is suspected of being immunologically mediated and idiosyncratic. It has a distinct presentation when compared to that ascribed to acute interstitial nephritis. The nephrotic syndrome is not associated with hemodynamically stressed patients. Recently Radford etal. [%] published a retrospective study of NSAIDs induced membranous nephropathy using the Mayo Clinic biopsy registry. They reported that >10% of biopsy proven membranous glomerulonephritis [stage I/II] was attributable to NSAIDs. They summarized the clinical features of... 

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