Authors: Mary A. Williamson Mt(ascp) Phd,L. Michael Snyder Md
Plasma rennin activity (PRA) in peripheral veins is often increased.
RENAL INFARCTION
Definition
Renal infarction commonly results from either thromboemboli, usually originating from clots in the heart or aorta, or an in situ renal artery thrombosis (less common).
Renal artery injury and atrial fibrillation are two common causes of renal infarction. Other causes include dissecting aneurysm of the aorta or renal artery, renal artery vasculitis (e.g., polyarteritis nodosa), or having hypercoagulable state (e.g., antiphospholipid syndrome).
Who Should Be Suspected
Candidates are patients with acute onset of flank or abdominal pain, frequently accompanied with nausea, vomiting, and fever.
Laboratory Findings
Urinalysis: microscopic or gross (less common) hematuria. Proteinuria may occur.
Plasma renin activity (PRA) may rise on the 2nd day and remain elevated for more than a month.
Increased serum creatinine concentration, particularity in patients with a large embolus.
Serum LDH is markedly increased (>400 U/L).
WBCs, CRP, and ESR are usually increased.
CT scan helps establish the diagnosis and asses the infarction.
RENAL TUBULAR ACIDOSIS
Renal tubular acidosis (RTA) refers to a group of disorders in which metabolic acidosis develops due to defects in the kidney’s ability to appropriately acidify the urine.