Lead nephropathy treatment

Scinchez-Fructuoso Al, Blanco J, Montserrat C, Ortega L, Arroyo M, Fernandez C, Prats D, Barrientos A. Experimental lead nephropathy treatment with calcium disodium ethylenediaminetetraacetate. Am J Kidney Dis 2002 40 59-67. Scinchez-Fructuoso Al, Toralbo A, Arroyo M, Lunque M, Ruilope LM, Santos JL, Cruceyra A, Barrientos A. Occult lead intoxication as a cause of hypertension and renal failure. Nephrol Dial Transplant 1996 11 1775-1780. 

Wedeen RP, Mallik DK. Batuman V. 1979. Detection and treatment of occupational lead nephropathy. Arch Intern Med 139 53-57. 

Selevan SG, Landrigan PJ, Stern FB, Jones JH. Mortality of lead smelter workers. Am J Epidemiol 1985 122 673-683. Wedeen RP, Mallik DK, Batuman V. Detection and treatment of occupational lead nephropathy. Arch Intern Med 1979 139 53-57. 

Khalil-Manesh, F., Gonick, H.C., Cohen, A., Bergamaschi, E., Mutti, A., 1992b. Experimental model of lead nephropathy. 11. Effeet of removal from lead exposure and chelation treatment with dimercaptosuccinic acid (DMSA). Environ. Res. 58, 35—54. 

Insulin is not a cure for diabetes. Patients with type 1 diabetes must take insulin throughout life. Proper treatment includes adherence to a diet and a program of physical exercise. There are serious long-term sequelae to diabetes if blood sugar levels are not adequately controlled blindness (retinopathy), kidney failure (nephropathy), and microvascular disease that can lead to heart attacks or amputations. 

In type 1 diabetes, diabetic nephropathy follows a predictable course from onset of diabetes to the onset of microalbuminuria to frank nephropathy to end-stage renal disease or death. Microalbuminuria (a tiny amount of protein in the urine) develops 10-14 years after onset of diabetes. Without treatment, clinical nephropathy follows within 5 years, and severe renal impairment leading to end-stage renal failure develops approximately 5 years later. Hypertension develops in association with microalbuminuria and progresses with diabetic nephropathy, further damaging the kidneys. Once end-stage renal disease (ESRD) is reached, the toxins in the body can no longer be cleared by the kidneys and, unless treated by dialysis, can build up to fatal levels. 

Cyclosporine is a macrolide antibiotic and has been used as an immunosuppressive agent. Cyclosporine can cause both renal and nonrenal toxicity. Clinically renal toxicity consists of four discrete syndromes which include acute reversible renal functional impairment, delayed renal allograft function, acute vasculopathy, and chronic nephropathy with interstitial fibrosis. Proximal tubular epithelium is uniquely sensitive to the toxic effect. The toxic effect is characterized by isometric cytoplasmic vacuolations (several small equally sized vacuoles in cytoplasm), necrosis with or without subsequent mineralization, inclusion bodies (giant mitochondria), and giant lysosomes. Acute vasculopathy consists of vacuolization of the arteriolar smooth muscles and endothelial cells leading to necrosis. In some cases, thrombotic microangiopathy develops, characterized by thrombosis of the renal micro vasculature. Long-term treatment with cyclosporine results in chronic nephropathy with interstitial fibrosis (Chamey et al., 2004). 

Metals A wide range of metals induce nephrotoxicity in humans and/or in animal models (Table 5). Some of these metals (e.g., iron, cobalt, copper) are essential elements required for normal body function, while others can be useful in treating diseases. For example, gold salts are useful in treating rheumatoid arthritis lithium salts are indicated for the treatment of manic-depressive illness and aluminum and bismuth salts are available to treat indigestion and stomach aches. However, exposure to these and other metals can occur from environmental sources and in excessive concentrations, can lead to nephropathy. 

ALDOSE REDUCTASE INHIBITORS (ARI) act at the enzyme aldose reductase, which is the first enzyme in the sorbitol (or polyol) pathway which converts glucose to sorbitol. It is thought that in hyperglycaemic states there may be an accumulation of sorbitol, leading to hyperosmotic pathology. ARI agents are under trial for use in the treatment of peripheral diabetic neuropathies, retinopathy and nephropathies. (These include tolrestat. also alrestatin, sorbinil, zenarestat and zopolrestat)... 

Reactions following initial infusions of antibody are common, but these can usually be handled by a cautious rate of infusion, appropriate hydration and diuresis, and, if necessary, praned-ication. Twenty six percent of initial reactions are reported to be mild, 48 % moderate, and 26 % severe. The initial infusion reaction to some mAbs, for example, rituximab (see below), may provoke tumor lysis syndrome, cytokine release syndrome, and systemic inflammatory response syndrome. Tumor lysis syndrome, noted particularly with rituximab, can occur following cancer treatment and sometimes without treatment. It is believed to be the result of breakdown products of cancer cells leading to increased levels of some metabolites and reflected in conditions such as hypercalcemia, hyperkalemia, hyperphosphatemia, acute uric acid nephropathy, and acute renal failure. The syndrome can occur in the early stages of mAb therapy and is potentially life-threatening. Cytokine release syndrome, also called cytokine storm, is commonly seen after... 

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