Renal Tubular Acidosis Type Iv
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Contents |
Etiology
- acquired condition generally caused by insufficient urinary buffers, generally NH3
- disorders of aldosterone metabolism (> 98% are associated with diabetes mellitus)
- hyporeninemic hypoaldosteronism
- resistance to aldosterone
- isolated aldosterone deficiency
- low renin, low aldosterone
- high renin, low aldosterone
- heparin
- ACE inhibitors
- angiotensin II receptor antagonists
- ketoconazole
Epidemiology
- most common form of RTA
Pathology
Clinical-manifestations
- no osteomalacia
- no nephrolithiasis
Laboratory
- Urine pH: < 5.5 (usually)
- serum HCO3-: > 15 meq/L
- serum aldosterone normal, high or low
- hyperkalemia
- normal 24 hour urine citrate
- generally decreased glomerular filtration rate
- azotemia (increased BUN & creatinine)
Radiology
- abdominal ultrasound if obstructive uropathy is suspected
Management
- rule out obstructive uropathy - foley catheter
- correct hyperkalemia [3]
- K+ restriction to 40-60 meq/day & a loop diuretic
- kayexelate may be necessary
- HCO3- 1.5-2.0 meq/kg/day may be required
- Fludrocortisone ( Florinef) 0.1-0.2 mg PO QD should be considered in patients with primary adrenal insufficiency
- stop ACE inhibitor
More General Terms
References
- Manual of Medical Therapeutics, 28th ed, Ewald & McKenzie (eds), Little, Brown & Co, Boston, 1995
- Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 603, 625
- Medical Knowledge Self Assessment Program (MKSAP) 11, 15, American College of Physicians, Philadelphia 1998, 2009
- Harrison's Principles of Internal Medicine, 13th ed. Isselbacher et al (eds), McGraw-Hill Inc. NY, 1994, pg 1324
