Year : 2012 | Volume
: 23 | Issue : 5 | Page : 1035--1037
Distal renal tubular acidosis in a child with HIV infection
Preeti Shanbag, Vaishali More, Jane David
Division of Pediatric Nephrology, Department of Pediatrics, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai, India
Division of Pediatric Nephrology, Department of Pediatrics, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai
Renal tubular acidosis (RTA) is not uncommon in HIV-infected children with advanced disease, and has been described mainly due to nephrotoxic anti-retroviral therapy and in association with prophylaxis or treatment of Pneumocystis carinii pneumonia with co-trimoxazole. We describe an 8-year-old boy, newly diagnosed to have HIV infection, who presented with distal RTA. There were no features of chronic RTA in the form of rickets or nephrocalcinosis, making an inherited form unlikely.
|How to cite this article:|
Shanbag P, More V, David J. Distal renal tubular acidosis in a child with HIV infection.Saudi J Kidney Dis Transpl 2012;23:1035-1037
|How to cite this URL:|
Shanbag P, More V, David J. Distal renal tubular acidosis in a child with HIV infection. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2021 Dec 5 ];23:1035-1037
Available from: https://www.sjkdt.org/text.asp?2012/23/5/1035/100944
HIV-associated nephropathy represents a disease spectrum that includes mild-to-moderate persistent proteinuria, hematuria, renal tubular acidosis (RTA) and end-stage renal disease. The prevalence varies and is associated with how advanced the immunosuppression is. , RTA defects have been reported in HIV patients previously, mainly in the context of nephrotoxic antiretroviral therapy and prophylactic co-trimoxazole treatment.  Distal RTA has been reported in an adult woman with HIV infection, acquired immunodeficiency syndrome (AIDS) and hypergammaglobulinemia.  We describe a child with distal RTA primarily due to HIV infection.
An 8-year-old boy was admitted with a history of fever, diarrhea and poor feeding for four days, and breathlessness and altered sensorium for one day. The child had been passing two to three loose stools per day. There was a history of repeated episodes of fever, cough and diarrhea in the past one year. Two months earlier, he had been investigated elsewhere and diagnosed to have pulmonary tuberculosis. Accordingly, anti-tuberculous therapy with isoniazide, rifampicin and pyrazinamide was started. The mother had died six months earlier of pulmonary tuberculosis and had been diagnosed to be HIV positive, probably following a blood transfusion during pregnancy. The father was HIV negative and he had been counseled to do the HIV testing in this child, but had not yet done it.
At admission in our hospital, the child was drowsy. The pulse was 120/min and peripheral pulses were well felt. Systolic blood pressure was 80 mmHg. The respiratory rate was 44/min. The breathing pattern was deep, suggesting Kussmaul's respiration. The child was dehydrated and had extensive oral thrush. The patient's weight was 20.5 kg (5 th percentile for age) and height 120 cm (10 th percentile for age). Grade 3 clubbing was present. There was no significant lymph node enlargement and no evidence of rickets or otitis media. Central nervous system examination revealed a drowsy arousable child. There was no focal neurological deficit and no signs of meningeal irritation. Examination of the respiratory system detected bilateral coarse crepitations. Abdominal examination showed a liver palpable 2 cm below the costal margin and spleen palpable 2 cm in its long axis from the costal margin. The impression at admission was acute gastroenteritis with dehydration and acidosis, and bronchopneumonia.
Laboratory investigations revealed a hemoglobin level of 8.5 g/dL and a white cell count of 13,000 WBC/mm 3 with a differential of polymorphs 58%, lymphocytes 32%, monocytes 6% and band forms 4%. The random blood sugar was 115 mg/dL, blood urea nitrogen was 20 mg/dL and serum creatinine 0.8 mg/dL. The arterial blood gases showed a pH of 7.157, pCO 2 16.3 mmHg, pO 2 119.4 mmHg, HCO 3 5.5 mmol/L and SaO 2 of 96.8%. Serum electrolytes revealed a sodium level of 138 mmol/L, potassium of 1.84 mmol/L and chloride of 118 mmol/L. Urinary electrolytes showed a sodium level of 120 mmol/L, potassium of 8.4 mmol/L and chloride of 72 mmol/L. Urine examination showed a pH level of 7.6, trace proteins and WBCs 2-3/hpf. Urinary calcium/ creatinine ratio was <0.2. Total proteins level was 8.8 g/dL, serum albumin of 3.6 g/dL and serum globulin of 5.2 g/dL; liver function tests were otherwise normal. Serum calcium was 8.9 mg/dL, inorganic phosphorus 4.8 mg/dL and alkaline phosphatase 120 U/L. Urinary screening for aminoaciduria and glucose was negative. Cerebrospinal fluid examination was normal. The Mantoux test showed no induration. Chest X-ray revealed patchy opacities in both lung fields with early bronchiectatic changes in both bases. Ultrasonogram of the abdomen revealed retroperitoneal lymph nodes. The kidneys were normal sized and there was no nephrocalcinosis. Blood, urine and stool cultures were sterile.
The patient's HIV-1 enzyme-linked immunosorbent assay was positive with three different kits. His CD4 count was 256/mm 3 and CD4 percentage of 15.9. Hepatitis B surface antigen and hepatitis C virus antibody were negative.
The patient was rehydrated with intravenous fluids supplemented with potassium chloride. Fluconazole was given to treat the oral candidiasis. Intravenous cefotaxime and amikacin were also started for the respiratory infection. Despite adequate rehydration and the subsiding diarrhea, the child continued to have persistent metabolic acidosis, which necessitated correction with intravenous sodium bicarbonate. With these measures there was a gradual improvement over the following week. The child required continuing therapy with oral potassium and sodium bicarbonate and was discharged with these supplements on Day 16 of admission. Antituberculous therapy was continued. Cotrimoxazole prophylaxis was started and the patient referred to the (anti-retroviral therapy (ART) center. At follow-up, one month later, the child gained 1.8 kg, but required potassium and sodium bicarbonate supplements to maintain normal serum potassium levels and a normal arterial blood gas profile.
We have described a case of RTA in a patient with HIV infection. The acidosis was hyper-chloremic, with a normal anion gap, and persisted despite correction of dehydration, cessation of diarrhea and normal renal function. In distal RTA, there is an inability to excrete hydrogen ions along the distal tubule. Hence, an inability to lower the urine pH to less than 5.5 in the presence of systemic acidosis suggests a diagnosis of distal RTA.  Measurement of the urinary anion gap (Na + + K+ Cl -) has been suggested for an initial evaluation of hyperchloremic metabolic acidosis; a positive anion gap suggests a decrease in distal urinary acidification.  In our patient, the presence of alkaline urine with the presence of severe acidosis and a positive urinary anion gap suggested distal RTA. Moreover, there were no features of a generalized Fanconi syndrome. There was no evidence of chronic RTA, such as rickets or nephrocalcinosis, suggesting that an inherited form of RTA was unlikely. RTA was probably secondary to the HIV infection.
Chakraborty et al found a 9% incidence of distal RTA in HIV-infected children. However, all these children were receiving ART. Many were also receiving co-trimoxazole (TMP) as prophylaxis against Pneumocystis carinii pneumonia. The hyperchloremic metabolic acidosis, renal bicarbonate wasting and growth failure was attributed to co-trimoxazole usage in these patients.  High doses of co-trimoxazole, as used in the treatment of Pneumocystis carinii pneumonia in AIDS patients, have the propensity to cause hyperkalemia by inhibiting sodium channels in the distal nephron, thereby impairing potassium secretion. , Hyperkalemia has also been observed in HIV-infected patients on standard doses used for prophylaxis.  Nephrogenic diabetes insipidus and renal tubular acidosis have been observed in HIV-infected patients, receiving foscarnet as therapy of cytomegalovirus infection.  Distal RTA has been described by Laing et al in an adult woman with HIV, AIDS and hyper-gammaglobulinemia.  Hyperglobulinemic states are a well-recognized cause of acquired distal RTA. Our patient also had hypergammaglobulinemia. Whether the distal tubular defect seen in our patient was due to the direct cytopathic effect of the virus on the renal tubules or secondary to hypergammaglobulinemia is not clear. Patients presenting with unexplained acquired RTA should be tested for HIV infection.
The authors would like to thank Dr. M.E. Yeolekar, Dean, Lokmanya Tilak Municipal Medical College and General Hospital, Mumbai, for permitting us to publish this manuscript. 
|1||Abuzaitoun OR, Hanson IC. Organ-specific manifestations of HIV disease in children. Pediatr Clin North Am 2000;47:109-125.|
|2||Connor E, Gupta S, Joshi V, et al. Acquired immunodeficiency syndrome-related renal disease in children. J Pediatr 1988;113:39-44.|
|3||Chakraborty R, Uy CS, Oleske JM, Coen PG, McSherry GD. Persistent non-gastro-intestinal metabolic acidosis in pediatric HIV-1 infection. AIDS 2003;17:673-7.|
|4||Laing CM, Roberts R, Summers S, Friedland JS, Lightstone L, Unwin RJ. Distal renal tubular acidosis in association with HIV infection and AIDS. Nephrol Dial Transplant 2006;21: 1420-2.|
|5||Barakat AY. Renal disease in children: Clinical evaluation and diagnosis. New York: Springer-Verlag; 1990.|
|6||Batlle DC, Hizon M, Cohen E, Gutterman C, Gupta R. The use of urinary anion gap in the diagnosis of hyperchloremic metabolic acidosis. N Eng J Med 1988;318:594-9.|
|7||Laufer M, Scott GB. Medical management of HIV disease in children. Pediatr Clin North Am 2000;47:127-51.|
|8||Mihm LB, Rathbun RC, Resman-Targoff BH. Hyperkalemia associated with high-dose trimethoprim-sulfamethoxazole in a patient with the acquired immunodeficiency syndrome. Pharmacotherapy 1995;15:793-7.|
|9||Perazella MA, Mahnensmith RL. Trimethoprim-sulfamethoxazole: Hyperkalemia is an important complication regardless of the dose. Clin Nephrol 1996;46:187-92.|
|10||Navarro JF, Quereda C, Gallego N, Antela A, Mora C, Ortuno J. Nephrogenic diabetes insipidus and renal tubular acidosis secondary to foscarnet therapy. Am J Kidney Dis 1996;27: 431-4.|
|11||Morris RC Jr, Fudenberg HH. Impaired renal acidification in patients with hypergammaglobulinemia. Medicine (Baltimore) 1967;46:57-69.|