volume repletion carbonic anhydrase inhibitor (e.g. acetazolamide) to facilitate loss of HCO3- in urine saline resistant metabolic alkalosis remove source of aldosterone or glucocorticoid spironolactone
Parenchymal Kidney Diseases
Vascular Diseases of the Kidney LARGE VESSEL DISEASE Table 8. Summary of Vascular Diseases Large Vessel Disease
important, potentially reversible cause of renal failure Etiology abdominal trauma, surgery, embolism, vasculitis, extra-renal compression, hypercoagulable state, aortic dissection kidney transplant more vulnerable Signs and Symptoms (depend on presence of collateral circulation) fever, N/V, flank pain leukocytosis, elevated AST, ALP marked elevated LDH (LDH >4x upper limit of normal with minimal elevations in AST/ALT strongly suggestive) acute onset HTN (activation of RAAS) or sudden worsening of long-standing HTN renal dysfunction, e.g. elevated Cr (if bilateral, or solitary functioning kidney) Investigations renal arteriography (more reliable but risk of atheroembolic renal disease) contrast-enhanced CT or MR angiography, duplex Doppler studies (operator dependent) Treatment prompt localization of occlusion and restoration of blood flow anticoagulation, thrombolysis, percutaneous angioplasty or clot extraction, surgical thrombectomy medical therapy in the long-term to reduce risk (e.g. antihypertensives) 2. ISCHEMIC RENAL DISEASE (RENAL ARTERY STENOSIS) chronic renal impairment secondary to hemodynamically significant renal artery stenosis or microvascular disease significant cause of ESRD: 15% in patients over 50 yr old (higher prevalence if significant vascular disease) usually associated with large vessel disease elsewhere causes of renal artery stenosis atherosclerotic plaques (90%): proximal 1/3 renal artery, usually males >55 yr, smokers electrolytes, osmolality (gently rehydrate when needed, e.g. CHF) fibromuscular dysplasia (10%): distal 2/3 renal artery or segmental branches, usually young females (typical onset <30 yr) (gently rehydrate when needed, e.g. CHF) when there is decreased RBF, GFR is dependent on angiotensin II-induced efferent arteriolar constriction which raises the FF (GFR/RBF) most common cause of secondary HTN ("renovascular HTN"), 1-2% of all hypertensive patients etiology decreased renal perfusion of one or both kidneys leads to increased renin release and subsequent angiotensin production increased angiotensin raises blood pressure in two ways 1. causes generalized arteriolar constriction 2. release of aldosterone increases Na+ and water retention elevated blood pressure can in turn lead to further damage of kidneys and worsening HTN