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Table of Contents
Year : 2012  |  Volume : 16  |  Issue : 7  |  Page : 114-116

Type 1 renal tubular acidosis in a patient of Type 1 diabetes mellitus: Is it coincidence or coexistence?

Department of General Medicine, Sher-I-Kashmir Institute of Medical Sciences Medical College and Hospital, Srinagar, India

Date of Web Publication24-Mar-2012

Correspondence Address:
Muzafar Naik
Department of General Medicine, SKIMS MCH Bemina, Srinagar
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2230-8210.94251

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A 26-year-old male patient suffering from Type 1 diabetes mellitus got admitted with abdominal pain and high blood sugars. On further evaluation, he was found to have normal anion gap metabolic acidosis without ketonuria and urinary pH was alkaline. The patient was diagnosed as Type 1 renal tubular acidosis (RTA) (distal RTA) and was managed by alkali replacement in addition to control of blood sugars. The association of Type 1 RTA with Type 1 diabetes mellitus has been rarely reported in the literature. The association needs a different attention as diagnosis and management of diabetic ketoacidosis in such cases will be tricky. The case presented here is the first of its kind from our part of the world and second as far as English literature is concerned.

Keywords: Type 1 diabetes mellitus, Type 1 renal tubular acidosis, normal anion gap metabolic acidosis

How to cite this article:
Naik M, Bhat T, Naqash M, Wani M, Dar N, Shah Y. Type 1 renal tubular acidosis in a patient of Type 1 diabetes mellitus: Is it coincidence or coexistence?. Indian J Endocr Metab 2012;16, Suppl S1:114-6

How to cite this URL:
Naik M, Bhat T, Naqash M, Wani M, Dar N, Shah Y. Type 1 renal tubular acidosis in a patient of Type 1 diabetes mellitus: Is it coincidence or coexistence?. Indian J Endocr Metab [serial online] 2012 [cited 2021 May 11];16, Suppl S1:114-6. Available from: https://www.ijem.in/text.asp?2012/16/7/114/94251

   Introduction Top

Type 1 diabetes mellitus (T1DM) is an autoimmune disorder and individuals with this disorder are prone to develop high anion gap metabolic acidosis with ketonuria, known as diabetic ketoacidosis (DKA). We report a case of normal anion gap metabolic acidosis without ketonuria during the management of hyperglycemia in a patient of T1DM. The patient was diagnosed to have distal renal tubular acidosis (dRTA). Although T1DM and dRTA are both associated with autoimmune disorders, their coexistence has been very rarely reported. Our case represents the second of its kind to the best of our knowledge and emphasizes the need to screen for dRTA in patients of T1DM, justified by the fact that different treatment strategy will be required for the management of diabetic ketoacidosis in T1DM associated with dRTA.

   Case Report Top

Our patient was a 26-year-old male, a known case of T1DM for 6 years on insulin, who presented to our outpatient department (OPD) with complaints of epigastric pain, postprandial fullness, and nausea. The patient was not compliant with the treatment and was coming erratically for follow-up to the OPD. On examination, the patient was conscious, oriented, dehydrated, and had mild pallor. Examination revealed a pulse rate of 60/minute, blood pressure (BP) of 100/60 mm Hg, respiratory rate (RR) of 17 breaths/minute, and temperature of 98.6°F. He had bilateral posterior subcapsular cataract and acne on face. Systemic examination revealed tender epigastrium and absent deep tendon reflexes. Rest of the systemic examination was normal.

Investigations revealed the following: hemoglobin (Hb) 10.2 g/dL; total leukocyte count (TLC) 5.3 × 10 9 /L; differential leukocyte count (DLC): N 71%, L 20%, M 7.5%; platelet 273 × 10 9 /L; erythrocyte sedimentation rate (ESR) 24/1 st h; urea 37 mg/dL; creatinine 1.09 mg/dL; bilirubin 1.34 mg/dL; aspartate transaminase (AST) 34 U/L; alanine transaminase (ALT) 50 U/L; alkaline phosphatase (ALP) 450 U/L; total protein 5.9 g/dL; and albumin 3.7 g/dL. Initial blood sugar was 284 mg/dL. Arterial blood gas analysis revealed the following: pH 7.20, pO2 72 mm Hg, sO2 95 mm Hg, pCO2 36 mm Hg, Na + 137 mEq/L, K + 2.5 mEq/L, HCO3 12.1 mEq/L, Cl 116 mEq/L (100-112 mEq/L). Urine for ketone bodies was negative. His HbA1C was 11.8%. ECG and chest X-ray were normal. 24-hour urinary protein was 100 mg/dL. The USG abdomen was normal. Patient was initially managed with IV normal saline and potassium replacement. After initial resuscitation with IV fluids, and potassium replacement, the patient's blood sugar stabilized to 172 mg/dL random; however, metabolic acidosis and hypokalemia persisted. Then, the possibility of dRTA was thought of. Anion gap was calculated as Na − [HCO3 + Cl], which was normal: 137 − [12.1 + 116] = 8.9 mEq/L. Furthermore, urine pH was 6.0 even at a serum pH of 7.20. The patient was diagnosed as dRTA in view of normal anion gap metabolic acidosis with hypokalemia with inability to acidify urine in the presence of systemic metabolic acidosis. Meanwhile, the patient started tolerating oral intake and was started on oral feeds with pre-meal subcutaneous regular insulin. Subsequently, the patient was put on oral sodium bicarbonate tablets at a dose of 2 mEq/kg and oral potassium replacement. His metabolic acidosis and hypokalemia improved markedly. He was discharged with a final diagnosis of T1DM with dRTA.

   Discussion Top

T1DM is a less common type of diabetes found in younger age group. It is thought to be caused by interaction of genetic, environmental, and immunological factors, which leads to the pancreatic beta cell destruction. [1] T1DM is associated with many autoimmune diseases as almost 15-30% patients have autoimmune thyroid disease, 4-9% have celiac disease, and 0.5% have Addison's disease. [2],[3] T1DM is also a part of autoimmune polyglandular syndrome type 1 and 2. [4] Other uncommon associated autoimmune diseases include pernicious anemia, juvenile rheumatoid arthritis, psoriasis, vitiligo, etc. [2]

Type 1 RTA or dRTA is a rare disease which can be either inherited, [5] sporadic, [6] endemic, [7] or acquired secondary to a variety of conditions. The most common causes of secondary dRTA are autoimmune disorders like Sjögren syndrome, autoimmune thyroiditis, chronic active hepatitis, primary biliary cirrhosis, systemic lupus erythematosus, hypothyroidism, and vasculitis. [8],[9],[10],[11] It has been seen that in some patients dRTA may be possibly caused by autoantibody against renal collecting duct. [12],[13]

The clinical spectrum of dRTA in T1DM is similar to that of diabetic ketoacidosis complicating T1DM, except for urine pH >5.5 in the former and presence of ketonuria in the latter. However, the management of acidosis in dRTA is contrary to that in diabetic ketoacidosis due to the controversial role of alkali therapy in the latter situation. Although T1DM and dRTA are both associated with autoimmune disorders, their coexistence has rarely been reported. [14] Whether this coexistence is purely coincidental or is because of common autoimmune pathogenesis is unclear. Interestingly, till date, diabetic ketoacidosis complicating T1DM associated with dRTA has not been reported in literature as the diagnosis and management of such a case will be challenging because the results of most clinical trials do not support the routine use of bicarbonate replacement, [15],[16] as in one study in children which showed that its use was associated with increased risk of cerebral edema. [17] On the other hand, soda bicarbonate is the cornerstone therapy for management of hypokalemia due to dRTA, and without correction of hypokalemia, the use of insulin is contraindicated in diabetic ketoacidosis.

Therefore, it is necessary to first explore the possible mechanism involved in dRTA in T1DM in order to draw a definite association of the two autoimmune disorders and secondly plan a treatment strategy during diabetic ketoacidosis in a patient of T1DM associated with dRTA.

   References Top

1.Bach JF. New concepts of etiopathogenesis and treatment of insulin-dependent diabetes mellitus. Clin Rev Allergy Immunol 2000;19:217-25.   Back to cited text no. 1
2.Hanukoglu A, Mizrachi A, Dalal I, Admoni O, Rakover Y, Bistritzer Z, et al. Extrapancreatic autoimmune manifestations of Type 1 diabetes mellitus patients and their first degree relatives. Diabetes Care 2003;26:1235-40.   Back to cited text no. 2
3.Barker JM. Type 1 Diabetes-Associated autoimmunity; Natural history, genetic associations and screening. J Clin Endocrinol Metab 2006;91:1210-7.   Back to cited text no. 3
4.Eisenbarth GS, Gottileb PA. Autoimmune polyendocrine syndromes. N Engl J Med 2004;350:2068-79.  Back to cited text no. 4
5.DuBose TD Jr, Alpern RJ. Renal tubular acidosis. In: Scriver CR, Beaudet AL, Sly WS, Valle D, editors. The Metabolic and Molecular Basis of Inherited Disease. New York, NY: McGraw Hill; 1995. p. 3655-89.   Back to cited text no. 5
6.Koul PA, Saleem SM, Bhat D. Sopra-dic distal renal tubular acidosis and periodic hypokalaemic paralysis in Kashmir. J Intern Med 1993;233:463-6.  Back to cited text no. 6
7.Vasuvattakul S, Nimmannit S, Chaovakul V, Susaengrat W, Shayakul C, Malasit P, et al. The spectrum of endemic renal tubular acidosis in the northeast of Thailand. Nephron 1996;74:541-7.  Back to cited text no. 7
8.Caruana RJ, Buckalew VM Jr. The syndrome of distal (type 1) renal tubular acidosis. Clinical and laboratory findings in 58 cases. Medicine (Baltimore) 1988;67:84-99.  Back to cited text no. 8
9.Koul PA, Saleem SM. Chronic active hepatitis with renal tubular acidosis presenting as hypokalemic periodic paralysis and respiratory failure. Acta Paediatr Scand 1992;81:568-9.  Back to cited text no. 9
10.Koul PA, Wahid A, Shah BA. SLE presenting as distal renal tubular acidosis with hypokalemic respiratory failure. Saudi J Kidney Dis Transpl 2003;14:190-3.  Back to cited text no. 10
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11.Koul PA, Wahid A. Distal renal tubular acidosis and hypokalemic paralysis in a patient of hypothyroidism. Saudi J Kidney Dis Transpl 2011;22:1014-6.  Back to cited text no. 11
[PUBMED]  Medknow Journal  
12.Konishi K, Hayashi M, Saruta T. Renal tubular acidosis with autoantibody directed against renal collecting duct cells. N Engl J Med 1994;331:1593-4.  Back to cited text no. 12
13.Gaarder PI, Heier HE. A human autoantibody to renal collecting duct associated with thyroid and gastric autoimmunity and possibly renal tubular acidosis. Clin Exp Immunol 1983;51:29-37.  Back to cited text no. 13
14.Dymot JA, McKay GA. Type 1 (distal) renal tubular acidosis in a patient with Type 1 diabetes mellitus--not all cases of metabolic acidosis in Type 1 diabetes mellitus are due to diabetic ketoacidosis. Diabet Med 2008;25;114-5.  Back to cited text no. 14
15.Latif KA, Freire AX, Kitabchi AE, Umpierrez GE, Qureshi N. The use of alkali therapy in severe diabetic ketoacidosis. Diabetic Care 2002;25:2113-4.  Back to cited text no. 15
16.Kitabchi AE, Wall BM. Management of Diabetic ketoacidosis. Am Fam Physician 1999;60:455-64.   Back to cited text no. 16
17.Chua HR, Schneider A, Bellomo R. Bicarbonate in diabetic ketoacidosis - A systematic review. Ann Intensive Care 2011;1:23.  Back to cited text no. 17


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