Steroid induced renal failure

Hypertension is prevalent in most patients with ESRD/advanced CKD. The blood pressure frequently often rises early after kidney transplantation after saline loading interacts with initial high-dose immunosuppression. Long-term blood pressure is often easier to control after transplantation, as long as the individual achieves a good GFR. However, poorly controlled blood pressure is common among kidney transplant recipients [ 1-4 ]. In a single-center study, for example, only 5 percent of kidney transplant patients were normotensive, as defined by blood pressures less than 130/80 mmHg, as measured by ambulatory blood pressure monitoring [ 2 ].

Treatment: If a pancreatic or liver tumor is identified and able to be surgically excised, the skin lesions may normalize for an extended period of time, but because these tumors metastasize (spread to other areas of the body) quickly, surgery is not curative. In cases of end stage liver disease, surgery is not possible, and the goal of therapy is to increase quality of life and decrease uncomfortable skin lesions with supportive care and addressing the nutritional abnormalities. Supportive care includes supplementing protein and necessary minerals and enzymes through the diet and oral supplements or by weekly intravenous amino acid infusions that are performed in the hospital on an outpatient basis until improvement in the skin is noted. Unfortunately, despite the supportive care, the disease will progress.

In cases where uric acid levels are significantly elevated (>750 mmol/l) the use of allopurinol (20 mg/kg . q 24 hr) may reduce hepatic uric acid production, while the administration of anabolic steroids may reduce protein catabolism. In cases of pre-renal ARF, rehydration, restoration of circulatory volume and supportive therapy may be all that is necessary. In cases of post renal obstruction, renal stones and ureteral obstructions will often have to be surgically removed before urine flow can be reestablished. In cases of toxin induced nephropathy, identification and removal of the toxin from the environment and gastric lavage may be useful. In cases of suspected aminoglycoside toxicity all drug medication should stop and osmotic diuresis instigated to maintain renal perfusion once normal hydration status has been achieved. Acute hypercalcemia (from acute vitamin D3 overdose but not breeding females) can cause ischemic acute tubular necrosis through the development of nephrocalcinosis, and in such cases prednisolone, calcitonin and diuresis should be considered. Chronic renal damage can also lead to calcium salt deposition in soft tissues including the kidney due to an elevation in the solubility index. Acute renal disease due to infectious agents should be empirically treated with broad spectrum anti microbials until culture and sensitivity results are obtained. It is important to use drugs with a large safety margin as drug metabolism and excretion may be significantly affected.

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

Steroid induced renal failure

steroid induced renal failure

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

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