Chronic glomerular nephritis

The author has observed a marked hypogammaglobulinemia in patients with the nephrotic syndrome in both the West Indies and Nigeria. In these patients the serum IgG level may be less than 500 mg/100 ml, and the urine electrophoretic pattern may resemble that of a normal serum. The striking hypogammaglobulinemia which so frequently accompanies chronic glomerular nephritis is responsible for the superimposed infection that may occur in this condition. 

Extensive literature has accumulated concerning other forms of renal dysfunction during long-term lithium therapy, including chronic interstitial nephritis and minimal-change glomerulopathy with nephrotic syndrome. Some instances of decreased glomerular filtration rate have been encountered but no instances of marked azotemia or renal failure. 

The major pathologic presentation of solvent associated nephropathy is that of anti-glomerular basement membrane disease [39] but epimembraneous and subacute proliferative glomerulonephritis have also been demonstrated. In addition, Narvarte et al. [40] reported on a patient with ulcerative colitis in which chronic interstitial nephritis developed that later was attributed to long-term exposure to organic solvents. 

The pathogenesis includes dehydration secondary to nephrogenic diabetes insipidus, as well as direct proximal and distal tubular cell toxicity resulting in ATN. Chronic tubulointerstitial nephritis attributed to lithium is evidenced most commonly by biopsy findings of interstitial fibrosis, tubular atrophy, and glomerular sclerosis (Presne et al. 2003 SUva 2004). The pathogenesis may involve cumulative direct lithium toxicity since duration of therapy has correlated with the decline in the GFR. The major risk factor for AKI is an elevated lithium concentration, particularly in associatimi with dehydration. 

Interstitial nephritis is associated with chronic exposure to heavy metals, while hydrocarbon exposure has been associated epidemiologically with glomerular nephritis, particularly Goodpasture s disease. 

Feeding of BHC (10-1600 mg kg diet) for life span to rats resulted in decreased body weight and an increase in mortality at 800 mg kg and above. Fatty degeneration and focal necrosis of the liver were observed at higher doses. Chronic nephritis with glomerular fibrosis and hyaline deposits was seen in rats fed 800 mg kg diet BHC. 

Diseases of the kidney that are discussed in this section include (1) the uremic syndrome, (2) chronic kidney disease, (3) end-stage renal disease, (4) diabetic nephropathy, (5) hypertensive nephropathy, (6) glomerular diseases, (7) interstitial nephritis, (8) polycystic Iddney disease, (9) polycystic kidney disease, (10) toxic nephropathy, (11) obstructive uropathy, (12) tubular diseases, (13) renal calculi, and (14) cystinuria. In addition, this section also includes discussions on (1) prostaglandins and NS AIDS in kidney disease, (2) monoclonal light chains and kidney disease, and (3) urinary osmolality. 

---