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| LETTER TO EDITOR |
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| Year : 2016 | Volume
: 3
| Issue : 1 | Page : 29-30 |
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Recurrent Hyperkalemic Renal Tubular Acidosis and Hyponatremia in Diabetes Mellitus due to Aldosterone Resistance
Mansoor C Abdulla, Jemshad Alungal, Ram Narayan
Department of General Medicine, M.E.S. Medical College, Malappuram, Kerala, India
| Date of Web Publication | 1-Feb-2016 |
Correspondence Address:
Mansoor C Abdulla
Department of General Medicine, M.E.S. Medical College, Perinthalmanna, Malappuram - 679 338, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2394-2916.175403
How to cite this article:
Abdulla MC, Alungal J, Narayan R. Recurrent Hyperkalemic Renal Tubular Acidosis and Hyponatremia in Diabetes Mellitus due to Aldosterone Resistance. J Integr Nephrol Androl 2016;3:29-30 |
How to cite this URL:
Abdulla MC, Alungal J, Narayan R. Recurrent Hyperkalemic Renal Tubular Acidosis and Hyponatremia in Diabetes Mellitus due to Aldosterone Resistance. J Integr Nephrol Androl [serial online] 2016 [cited 2023 Mar 24];3:29-30. Available from: http://www.journal-ina.com/text.asp?2016/3/1/29/175403 |
Dear Editor,
Renal tubular acidosis (RTA) associated with hyperkalemia suggests a generalized dysfunction in the cortical and medullary collecting tubules attributable to real or apparent hypoaldosteronism. Diabetes and other interstitial diseases including amyloid, monoclonal gammopathies, and interstitial nephritis associated with nonsteroidal antiinflammatory agents result in hyporeninemic hypoaldosteronism. Functional hypoaldosteronism can be either inherited or due to various drugs that affect aldosterone activity, either directly by interference with its receptor or by affecting its target pathway.
A 70-year-old female presented with tiredness and fatigue for 2 days. She had diabetics for 10 years on glimepiride and metformin. She had a history of recurrent hospital admissions for hyperkalemia in the last 5 months. On examination, she was pale and the blood pressure was 130/80 mm Hg. She appeared adequately hydrated on clinical examination, and examination of respiratory, cardiovascular, neurological systems, and abdomen were unremarkable.
Hemoglobin was 10.7 g/dL, total white blood cell count 5600/μL, platelet count 200 × 10 9 /L, and erythrocyte sedimentation rate 39 mm in 1 h. Urinalysis showed 1-2 leukocytes/high power field. There was no albuminuria or visible red blood cell in the urine. Chest X-ray and electrocardiogram were normal. Her biochemical parameters revealed RBS 151 mg%, glycosylated hemoglobin 7.3, urea 28 mg/dL, creatinine 0.7 mg/dL, and uric acid 2.0 mg%. Tests for liver function, thyroid function, and serum cortisol were normal. The serum and urinary electrolytes and arterial blood gas analyzes are shown in [Table 1]. Urine culture was sterile, and ultrasonography of abdomen was normal. The transtubular potassium gradient was 3.12. The patient had hypoosmolar, euvolemic hyponatremia, and hyperkalemia with TTKG <7, normal anion gap metabolic acidosis and hypomagnesemia. Her TTKG was 4 after physiologic dosing of 9-alpha-fludrocortisone, suggesting aldosterone resistance, but after 3 days of 0.2 mg of 9-alpha-fludrocortisone, her TTKG was 10. Plasma aldosterone and renin levels were normal. She was continued on 0.2 mg of 9-alpha-fludrocortisone daily and oral magnesium supplements with which her electrolyte abnormalities were corrected. | Table 1: Serum and urinary electrolytes, and arterial blood gas analyzes
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The inability of the kidney either to excrete sufficient net acid or to retain sufficient bicarbonate, results in RTAs, which causes normal anion gap acidosis. [1] Among them, type IV is the only variant associated with hyperkalemia in which the collecting duct fails to excrete both protons and potassium. Thus, the presence of hyperkalemia with normal anion gap hyperchloremic acidosis indicates a state of generalized distal nephron dysfunction, which arises when aldosterone is insufficient either in quantity or activity. This may be genetic or acquired. In adults, hyperkalemic RTA often represents an acquired disorder causing mineralocorticoid deficiency, either as a primary adrenal disorder or as secondary to hyporeninemia in patients with mild to moderate renal insufficiency due to diabetic nephropathy, systemic lupus erythematosus, and AIDS nephropathy. Reduced responsiveness to aldosterone is usually associated with various tubulointerstitial renal diseases and drugs. [2] Diabetes causes hyperkalemia with normal anion gap hyperchloremic acidosis due to hyporeninemic hypoaldosteronism. Our patient had recurrent episodes of hyperkalemia with normal anion gap metabolic acidosis, which was probably due to reduced responsiveness to aldosterone evidenced by TTKG <6 after physiologic doses of mineralocorticoid and normal plasma aldosterone and renin levels. In patients with adrenal insufficiency after a physiologic dose of mineralocorticoid, the TTKG increases to more than 6 within 4 h, and in most cases within 2 h. [3] Zettle et al. described few patients who had aldosterone resistance whose TTKG did not increase to more than 6 after physiologic mineralocorticoid doses. However, some of them had delayed response to pharmacologic doses of mineralocorticoid. [4] Hyponatremia, hyperkalemia, and normal anion gap metabolic acidosis in our patient responded to pharmacologic doses of 9-alpha-fludrocortisone suggesting the causative role of aldosterone. Hypomagnesemia also might be secondary to diabetes in our patient. Hypomagnesemia occurs at an incidence of 13.5-47.7% among patients with type 2 diabetes due to various mechanisms. [5] Hypomagnesemia in diabetes can be due to decreased intake (esophageal dysfunction and diabetic gastroparesis), enhanced gastrointestinal loss (diarrhea secondary to autonomic dysfunction), and increased renal magnesium loss either due to enhanced filtered load or reduced renal reabsorption. Even though hyporeninemic hypoaldosteronism is well described in diabetes, a state of attenuated response to aldosterone secondary to diabetes resulting in multiple electrolyte abnormalities was not described previously. Reporting of such mechanisms will help explicate the pathophysiological aspects of various electrolyte abnormalities in diabetes and throws open the scope for more study and research.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | DuBose TD Jr. Acid-base disorders. In: Brenner BM, editor. Brenner and Rector's the Kidney. Vol. 1. Philadelphia: W.B. Saunders Co.; 2000. p. 948-62.  |
| 2. | Karet FE. Mechanisms in hyperkalemic renal tubular acidosis. J Am Soc Nephrol 2009;20:251-4. |
| 3. | Choi MJ, Ziyadeh FN. The utility of the transtubular potassium gradient in the evaluation of hyperkalemia. J Am Soc Nephrol 2008;19:424-6. |
| 4. | Zettle RM, West ML, Josse RG, Richardson RM, Marsden PA, Halperin ML. Renal potassium handling during states of low aldosterone bio-activity: A method to differentiate renal and non-renal causes. Am J Nephrol 1987;7:360-6. |
| 5. | Pham PC, Pham PM, Pham SV, Miller JM, Pham PT. Hypomagnesemia in patients with type 2 diabetes. Clin J Am Soc Nephrol 2007;2: 366-73. |
[Table 1]
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