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Calcific uremic arteriolopathy is a severe and life-threatening condition that develops in patients with kidney disease. Most commonly, it presents with skin rash and painful subcutaneous nodules. However, other organs may be involved. We report a case of a young man who developed renal failure in the transplanted kidney. Renal biopsy demonstrated myointimal calcification in the renal arteries consistent with this diagnosis.

Chronic lead nephropathy occurs as a result of years of lead exposure. This disease has been prevalent throughout human history. It is important that primary care providers and internists recognize this disorder because it can contribute to progressive loss of kidney function. Diagnosis is made by a thorough history in combination with physical examination. A history of lead intoxication often requires knowledge of the various sources of lead exposure. Laboratory tests, many previously known and some newly described, are available to further support this diagnosis. Therapy to reduce lead burden may be useful when employed early in the disease; new data sheds more light on which patients should be treated and when such patients should undergo chelation therapy. In particular, treatment with calcium EDTA chelation may benefit certain patients with chronic kidney disease by slowing the progression to end-stage renal disease.

The renin-angiotensin-aldosterone system (RAAS) plays an integral role in maintaining vascular tone, optimal salt and water homeostasis, and cardiac function in humans. However, it has been recognized in recent years that pathologic consequences may also result from overactivity of the RAAS. Clinical disease states such as renal artery stenosis, hypertension, diabetic and nondiabetic nephropathies, left ventricular hypertrophy, coronary atherosclerosis, myocardial infarction, and congestive heart failure (CHF) are examples. Part of the adverse cardiorenal effects of the RAAS may be related to the prominent role that this system plays in the activation of the sympathetic nervous system, the dysregulation of endothelial function and progression of atherosclerosis, as well as inhibition of the fibrinolytic system. Also, direct profibrotic actions of angiotensin II and aldosterone in the kidney and heart promote end organ injury. Current basic science and clinical research supports the use of inhibitors of the RAAS, including angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists in treating hypertension, improving diabetic nephropathy and other forms of chronic kidney disease, preventing or ameliorating CHF, and optimizing prognosis after myocardial infarction.