Exposure to heavy metals and other toxins can cause tubulointerstitial disorders.
Heavy metals (eg. As lead, cadmium, copper) and other toxins can cause a form of chronic interstitial nephritis.
Exposure to heavy metals and other toxins can cause tubulointerstitial disorders. Heavy metals (eg. As lead, cadmium, copper) and other toxins can cause a form of chronic interstitial nephritis. Lead-induced nephropathy Chronic tubulointerstitial nephritis is caused by accumulation of lead in the proximal tubular cells. Temporary Lead exposure leads to a proximal Tubulusdysfunktion with reduced Uratsekretion and hyperuricemia (urate is the substrate for lead gout), aminoaciduria and renal glycosuria. A chronic (eg., 5 to ? 30 years) lead exposure causes progressive tubular atrophy, and interstitial fibrosis with renal hypertension and gout. However, chronic exposure can lead to low levels independent of a tubulointerstitial disease to renal failure and hypertension. The following groups have the highest risk: children who leaded paint dust or lead-based paint chips are exposed, welders workers in battery factories those high-proof distilled consume ( “moonshine”) alcohol. Children with exposure can develop a nephropathy in adulthood. Common findings include a mild urinary sediment and hyperuricemia all proportion to the degree of renal impairment: Serum urate> 9 mg / dL with serum creatinine <1.5 mg / dl serum urate> 10 mg / dl with serum creatinine 1.5 to 2 mg / dl serum urate> 12 mg / dl with serum creatinine> 2 mg / dl the diagnosis is usually in the blood by measuring the lead content (total lead). Alternatively, one can demonstrate increased bone lead concentration by Ro-ray displaying a high cumulative exposure to lead. Chelation therapy can stabilize renal function, but the recovery remains incomplete. Cadmium Cadmium exposure nephropathy caused by contaminated water or food and tobacco -hauptsächlich- by Occupational exposure may trigger a nephropathy. It can also lead to a glomerulopathy which is usually asymptomatic. As an early manifestation of a Kadmiumnephropathie signs of tubular dysfunction occur (eg. As beta-2 microglobulin), aminoaciduria and renal glucosuria including a low molecular tubular proteinuria. The symptoms and complaints that occur due to chronic kidney disease. The kidney failure follows a dose-response relationship. The following makes the diagnosis of Kadmiumnephropathie likely: Past exposure to cadmium in the workplace Increased concentrations of beta-2-microglobulin in urine (not detect through urine protein measurement with test strips, but by radioimmunoassay) Increased cadmium concentration in urine (> 7 micrograms / g creatinine) Treatment is the removal of cadmium exposure; note that chelation may worsen renal toxicity in acute cadmium poisoning with EDTA, but has been used successfully in chronic cadmium exposure. The tubular proteinuria is usually irreversible. Other Schwermetallnephropathien The other heavy metals which are nephrotoxic include, copper gold Urani arsenic iron mercury bismuth chromium All of these metals cause tubular injury and dysfunction (z. B. tubular proteinuria, aminoaciduria), further comprising a tubular necrosis. For some substances (mercury, gold) but a glomerulopathy can stand in the foreground. The treatment includes the patient’s removal from further exposure and one or both of the following: chelating agents (copper, arsenic, bismuth) Dialysis (chromium, arsenic, bismuth) is often used when the chelation fails or simultaneously with chelation in severe arsenic poisoning