Renal tubular acidosis: Difference between revisions
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*Diagnostic classification starts with low, normal, or high serum potassium | *Diagnostic classification starts with low, normal, or high serum potassium | ||
*Differentiate from [[uremia]] in which acidosis is anion gap | *Differentiate from [[uremia]] in which acidosis is anion gap | ||
==Differential== | |||
*See [[metabolic acidosis]] | |||
==Workup== | |||
*ABG or VBG | |||
*BMP, phos, mag | |||
*Urine pH | |||
*Urine electrolytes - Na, K, Cl, Ca, Cr | |||
*Plasma aldosterone and cortisol for type IV RTA | |||
*Note that when hyperkalemia is present, aldosterone should be elevated, so a "normal" aldosterone level may be relatively low | |||
==Etiologies== | |||
*Type II RTA | |||
**[[Multiple myeloma]] | |||
**[[Amyloidosis]] | |||
**Drugs - ifosfamide, [[acetazolamide]] | |||
**Heavy metals ([[Lead]], mercury, copper/Wilson's) | |||
**Vitamin D deficiency, rickets, hypophosphatemia | |||
**[[Paroxysmal nocturnal hemoglobinuria]] | |||
**Renal transplant | |||
**Fanconi's syndrome | |||
**Familial | |||
**Primary metabolic (cystinosis, von Gierke's) | |||
*Type I RTA | |||
**Autoimmune - [[Sjogren's]], [[SLE]], [[RA]] | |||
**Drugs - [[Lithium]], [[amphotericin B]], ifosfamide | |||
**[[Sickle cell disease]] | |||
**[[Cirrhosis]] | |||
**Obstructive uropathy | |||
**Renal transplant | |||
**Familial (decreased H+/K+-ATPase, Na+/K+-ATPase activity) | |||
*Type IV RTA | |||
**Aldosterone deficiency or resistance | |||
**Diabetic nephropathy (hyporenin/hypoaldosteronism) | |||
**Obstructive uropathy | |||
**Chronic tubulointerstitial disease | |||
**Potassium-sparing diuretics | |||
**Heparin induced adrenal insufficiency | |||
==Features and Treatment== | |||
*Mild acidosis in adults with bicarb > 20 mEq/L may not require Tx | |||
*Children should be treated due to impaired growth | |||
*For type I and II RTA, treat all children and infants | |||
**Generally, 5-15 mEq/kg/day oral bicarbonate | |||
**May require IV bicarbonate for severe acidosis | |||
**PO potassium supplements | |||
**Treat adults with bicarb < 18-20 mEq/L | |||
**Treat underlying d/o (Vitamin D, etc.) | |||
===Proximal Tubular Acidosis=== | |||
*Type II RTA - reduced bicarbonate reabsorption | |||
**[[Hypokalemia]] | |||
**Serum bicarb 12-20 mEq/L generally | |||
**Urine pH < 5.5, but can be variable | |||
*Urine pH > 5.5 if undergoing alkali therapy | |||
===Distal Tubular Acidosis=== | |||
*Type I RTA - impaired H+ and ammonium secretion | |||
**[[Hypokalemia]] | |||
***Normokalemia may be seen in chronic interstitial renal disease | |||
**Serum bicarb may be < 10 mEq/L | |||
**Urine pH > 5.5 | |||
**Urinary anion gap > 50 mEq/L = Na + K - Cl | |||
**[[Nephrolithiasis]], calcium stones from chronic acidosis causing bone resorption and hypercalciuria | |||
===Type IV RTA=== | |||
*Also distal tubular acidosis | |||
**[[Hyperkalemia]] | |||
**Mild acidosis, with bicarb generally > 17 mEq/L | |||
**Urine pH < 5.5 | |||
*Serum aldosterone and cortisol levels to determine between: | |||
**Adrenal insufficiency, Addison's (low aldosterone, low cortisol) | |||
**Selective aldosterone deficiency (low aldosterone, normal cortisol) | |||
**Aldosterone resistance (nl to high aldosterone, nl to high cortisol) | |||
==Sources== | ==Sources== |
Revision as of 21:40, 2 May 2016
Background
- Hyperchloremic metabolic acidosis, non-anion gap
- Diagnostic classification starts with low, normal, or high serum potassium
- Differentiate from uremia in which acidosis is anion gap
Differential
Workup
- ABG or VBG
- BMP, phos, mag
- Urine pH
- Urine electrolytes - Na, K, Cl, Ca, Cr
- Plasma aldosterone and cortisol for type IV RTA
- Note that when hyperkalemia is present, aldosterone should be elevated, so a "normal" aldosterone level may be relatively low
Etiologies
- Type II RTA
- Multiple myeloma
- Amyloidosis
- Drugs - ifosfamide, acetazolamide
- Heavy metals (Lead, mercury, copper/Wilson's)
- Vitamin D deficiency, rickets, hypophosphatemia
- Paroxysmal nocturnal hemoglobinuria
- Renal transplant
- Fanconi's syndrome
- Familial
- Primary metabolic (cystinosis, von Gierke's)
- Type I RTA
- Autoimmune - Sjogren's, SLE, RA
- Drugs - Lithium, amphotericin B, ifosfamide
- Sickle cell disease
- Cirrhosis
- Obstructive uropathy
- Renal transplant
- Familial (decreased H+/K+-ATPase, Na+/K+-ATPase activity)
- Type IV RTA
- Aldosterone deficiency or resistance
- Diabetic nephropathy (hyporenin/hypoaldosteronism)
- Obstructive uropathy
- Chronic tubulointerstitial disease
- Potassium-sparing diuretics
- Heparin induced adrenal insufficiency
Features and Treatment
- Mild acidosis in adults with bicarb > 20 mEq/L may not require Tx
- Children should be treated due to impaired growth
- For type I and II RTA, treat all children and infants
- Generally, 5-15 mEq/kg/day oral bicarbonate
- May require IV bicarbonate for severe acidosis
- PO potassium supplements
- Treat adults with bicarb < 18-20 mEq/L
- Treat underlying d/o (Vitamin D, etc.)
Proximal Tubular Acidosis
- Type II RTA - reduced bicarbonate reabsorption
- Hypokalemia
- Serum bicarb 12-20 mEq/L generally
- Urine pH < 5.5, but can be variable
- Urine pH > 5.5 if undergoing alkali therapy
Distal Tubular Acidosis
- Type I RTA - impaired H+ and ammonium secretion
- Hypokalemia
- Normokalemia may be seen in chronic interstitial renal disease
- Serum bicarb may be < 10 mEq/L
- Urine pH > 5.5
- Urinary anion gap > 50 mEq/L = Na + K - Cl
- Nephrolithiasis, calcium stones from chronic acidosis causing bone resorption and hypercalciuria
- Hypokalemia
Type IV RTA
- Also distal tubular acidosis
- Hyperkalemia
- Mild acidosis, with bicarb generally > 17 mEq/L
- Urine pH < 5.5
- Serum aldosterone and cortisol levels to determine between:
- Adrenal insufficiency, Addison's (low aldosterone, low cortisol)
- Selective aldosterone deficiency (low aldosterone, normal cortisol)
- Aldosterone resistance (nl to high aldosterone, nl to high cortisol)
Sources
- Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock. Renal Tubular Acidosis Syndromes. South Med J. 2000;93(11). http://www.medscape.com/viewarticle/410658.