Renal function impairment nephropathy

Renal function impairment Renal impairment, including minimal change nephropathy, and acute and chronic interstitial nephritis, has occurred. 

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). 

Seldom are renal parenchymal abnormalities consistent with RPD picked up as an incidental finding on a US, CT or MRl study performed because of a different query, such as interstitial (septic) renal involvement and parainfectious GN in a septic patient, or RPD in a dystrophic child. Contrast-enhanced CT studies may demonstrate delayed and prolonged parenchymal enhancement with reduced cortico-medullary differentiation of enlarged kidneys in acute GN. In general radiopaque intravenous contrast as administered for IVU or CT should be avoided in RPD with renal functional impairment if these studies are performed, good hydration as well as diuretic measures are compulsory to prevent possible contrast nephropathy with renal damage such as papillary necrosis or even renal failure (Erley and Bader 2000 Morcos 1998 Murphy et al. 2000). 

Allopurinol is the antihyperuricemic drug of choice in patients with a history of urinary stones or impaired renal function, in patients who have lymphoproliferative or myeloproliferative disorders and need pretreatment with a xanthine oxidase inhibitor before initiation of cytotoxic therapy to protect against acute uric acid nephropathy, and in patients with gout who are overproducers of uric acid. 

Renal function /mpa/rmenf Anuria, acute or chronic renal insufficiency and evidence of diabetic nephropathy are contraindications because potassium retention is accentuated and may result in the rapid development of hyperkalemia. Do not give to patients with evidence of renal impairment (BUN greater than 30 mg/dL or serum creatinine greater than 1.5 mg/dL) or diabetes mellitus without continuous monitoring of serum electrolytes, creatinine, and BUN levels. 

Renai function impairment Perform periodic BUN and serum potassium determinations to check kidney function, especially in patients with suspected or confirmed renal insufficiency and in elderly or diabetic patients diabetic patients with nephropathy are especially prone to develop hyperkalemia. 

Barrett BJ, Parfrey PS, Vavasour HM, et al, Contrast nephropathy in patients with impaired renal function high versus low osmolar media. Kidney Int 1992 41 1274-1279. 

The results of two trials in patients with chronic nephropathy have reinforced the benefit of ACE inhibitors in slowing the progression of chronic renal insufficiency due to renal diseases other than diabetic nephropathy (13-15) and have provided sufficient information on the safety profile of these agents in chronic renal insufficiency. This was found to be essentially the same as in patients with normal renal function. The current practice of avoiding ACE inhibitors in severe renal insufficiency, to prevent further renal impairment and hyperkalemia, is no longer justified, although careful monitoring should still be observed. 

Under normal conditions each of the two million nephrons of the kidney work in an organized approach to filter, reabsorb, and excrete various solutes and water. The kidney is a primary regulator of sodium and water as well as acid-base homeostasis. The kidney also produces hormones necessary for red blood cell synthesis and calcium homeostasis. Impairment of normal kidney function is often referred to as renal insufficiency. Based on the time course of development, renal insufficiency has historically been divided into two broad categories. Acute renal failure (ARF) refers to the rapid loss of renal function over days to weeks. Chronic kidney disease (CKD)", also called chronic renal insufficiency (CRI) by some, is defined as a progressive loss of function occurring over several months to years, and is characterized by the gradual replacement of normal kidney architecture with interstitial fibrosis. Progressive kidney disease or nephropathy is... 

Allopurinol is the antihyperuricemic drug of choice in patients with a history of urinary stones or impaired renal function, in patients who have lymphoproliferative or myeloproliferative disorders and need pretreatment with a xanthine oxidase inhibitor before initiation of cytotoxic therapy to protect against acute uric acid nephropathy, and in patients with gout who are overproducers of uric acid. The major side effects of allopurinol are skin rash, leukopenia, occasional gastrointestinal toxicity, and increased frequency of acute gouty attacks with the initiation of therapy. An allopurinol hypersensitivity syndrome characterized by fever, eosinophilia, dermatitis, vasculitis, and renal and hepatic dysfunction is a rare side effect, but is associated with a 20% mortality rate. ... 

The prevention of urate nephropathy might be a stronger indication because it is irreversible even with proper treatment. Available data indicate, however, that gouty nephropathy is extremely rare in the absence of clinical gout, and evidence that elevation of uric acid by itself may cause renal disease is weak and inconclusive. As discussed previously, renal impairment is very rare in the absence of concurrent hypertension and atherosclerosis. In addition, it is unclear whether uric acid-lowering therapy protects renal function in such individuals. Available data thus do not justify therapy for most patients with asymptomatic hyperuricemia. 

Mofetil mycophenolate is a noncompetitive, reversible, inhibitor of inosine monophosphate dehydrogenase that inhibits lymphocyte proliferation. The use of mofetil mycophenolate with concomitant CsA dose reduction or withdrawal has showed to be safe in terms of acute rejection and in many times to induce rapid and significant improvements in renal function and hemodynamics in renal transplant recipients with stable or impaired renal function [337-340] and stable hver or heart transplant recipients with renal dysfunction [341-343]. David-Neto et al retrospectively analyzed a group of 13 renal transplanted children with biopsy showing chronic transplant nephropathy whom had CsA dose reduced or withdrawn and azathiopiine switched to mofetil mycophenolate. Six months after the introduction of mofetil mycophenolate median serum creatinine decreased from values of 2.2 mg/dl to... 

Barrett BJ, Parfrey PS, Vavasour HM, McDonald J, Kent G, Hefferton D, O Dea F, Stone E, Reddy R, McManamon PJ. Contrast nephropathy in patients with impaired renal function high versus low osmolar media. Kidney Int 1992 41 1274-1279. Rudnick MR, Berns JS, Cohen RM, Goldfarb S. Contrast media-associated nephrotoxicity. Curr Opin Nephrol Hypert 1996 5 ... 

---