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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2018  |  Volume : 29  |  Issue : 5  |  Page : 1216-1219
An initial evaluation of hypokalemia turned out distal renal tubular acidosis secondary to parathyroid adenoma


1 Department of Nephrology, Jawaharlal Nehru Medical College, Sawangi, Wardha, Maharashtra, India
2 Janta Hospital, Nagpur, Maharashtra, India
3 Department of Cardiology, Jawaharlal Nehru Medical College, Sawangi, Wardha, Maharashtra, India
4 Department of Medicine, Northern Railway Central Hospital, New Delhi, India
5 Children's Hospital, Michigan, USA
6 Department of Nephrology, Government Medical College and Super Specialty Hospital, Nagpur, Maharashtra, India

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Date of Submission02-Oct-2017
Date of Decision08-Dec-2017
Date of Acceptance13-Dec-2017
Date of Web Publication26-Oct-2018
 

   Abstract 

Primary hyperparathyroidism (PHPT) usually presents with hypercalcemia related symptoms and signs. Kidneys play an important role in calcium homeostasis. PHPT has been reported to be associated with hyperchloremia, defective urinary acidification, and renal tubular acidosis (RTA). The dysfunction of distal renal tubules is proposed to be secondary to calcium deposition in distal tubules. This case report highlights an initial presentation of parathyroid adenoma as hypokalemia due to distal RTA secondary to medullary nephrocalcinosis.

How to cite this article:
Balwani MR, Pasari A, Meshram A, Jawahirani A, Tolani P, Laharwani H, Bawankule C. An initial evaluation of hypokalemia turned out distal renal tubular acidosis secondary to parathyroid adenoma. Saudi J Kidney Dis Transpl 2018;29:1216-9

How to cite this URL:
Balwani MR, Pasari A, Meshram A, Jawahirani A, Tolani P, Laharwani H, Bawankule C. An initial evaluation of hypokalemia turned out distal renal tubular acidosis secondary to parathyroid adenoma. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2018 Dec 15];29:1216-9. Available from: http://www.sjkdt.org/text.asp?2018/29/5/1216/243965

   Introduction Top


Kidneys play an important role in calcium homeostasis via regulation of active 1,25-dihyroxy Vitamin D synthesis. Parathyroid hormone receptors are expressed widely across renal tubules, where it helps in calcium reabsorption and endocrine function.[1] Primary hyperparathyroidism (PHPT) usually manifests as hypercalcemia related signs and symptoms. This hypercalcemia is in part caused by increased tubular reabsorption of calcium. Other manifestations of hyperparathyroidism include hypophosphataemia due to decreased tubular phosphate reabsorption, metabolic acidosis due to reduced tubular bicarbonate reabsorption and increased serum 1,25-dihydroxy- Vitamin D secretion. Increased active Vitamin D secretion, in turn, leads to enhanced absorption of dietary calcium. Hypercalciuria occurs due to the combined effects of increased calcium reabsorption and bone resorption.[1] Defective acidification of urine and renal tubular acidosis (RTA) have been reported in the past to be associated with primary hyperparathyroidism.[2] Nephrolithiasis is seen in distal RTA, where there is a defect in acidi- fication of urine due to loss of generation and maintenance of a hydrogen ion gradient by the distal tubular cells.[3] The proposed mechanism leading to dysfunction of distal tubular cells has been linked to hypercalciuria.[4] The filtered load of calcium in the glomerulus increases proportionately with the degree of serum hypercalcemia. Hypercalciuria is one of the evident factors in the complex pathophysiology of the renal stone formation. Most renal stones in patients with PHPT are composed of calcium oxalate, although slightly alkaline urine may favor the precipitation of calcium phosphate stones. The following case report highlights a case of PHPT due to solitary parathyroid adenoma which initially presented with symptoms of hypokalemia due to renal tubular acidosis and medullary nephrocalcinosis probably secondary to hypercalcemia.


   Case Report Top


We present a case of a 37-year male who had a six-month history of generalized weakness, myalgia, and nocturia. There was no history of fever, rash, joint pain, abdominal pain, hematuria, or diarrhea. Systemic examination revealed no significant abnormality. Power was normal in all four limbs with normal reflexes. His initial biochemistry which was performed three months back revealed hypo-kalemia (k- 2.9 mEq/L) with deranged kidney function tests (urea – 48 mg/dL, creatinine – 1.8 mg/dL). He was referred for evaluation of the same at our institute. Initial systemic examination including genitourinary system revealed no significant abnormality. Laboratory examination again revealed hypokalemia (K – 2.8 meq/L) and deranged kidney functions (urea – 22.94 mg/dL, creatinine – 1.5 mg/dL). He was labeled as chronic kidney disease and referred to nephrologist for further evaluation. The patient was not on any diuretics. Initial evaluation by nephrologist revealed following: urine pH – 7, arterial blood gases showed pH 7.28, PaO2 106 mm Hg, Pa CO2 34mm Hg, bicarbonate 17mmol/L, and SaO2 98%. Serum anion gap was 10. Thus, a diagnosis of distal RTA was kept in view of hyperchloremic metabolic acidosis with normal anion gap. In between, ultrasonography abdomen revealed typical papillary calcifications in the form of hyper-echoic foci with acoustic shadowing at the tips of the pyramids which was suggestive of bilateral medullary nephrocalcinosis. Further evaluation revealed incidental hypercalcemia (serum calcium – 13.1 mg/dL), hypophosphatemia (serum PO4 – 1.8 mg/dL). Afterward, intact parathyroid hormone was performed which came to be borderline high (serum iPTH – 89.2 pg/mL). Thyroid function tests and 25 OH Vitamin D levels were within normal limits. Thus, provisonal diagnosis of PHPT induced hypercalcemia and medullary nephrocalcinosis was kept. This medullary nephrocalcinosis would have led to distal RTA induced hypokalemia. Nuclear scan (Tc 99 M-sestamibi) confirmed left inferior parathyroid adenoma [Figure 1]. This ultimately led to the diagnosis of PHPT due to parathyroid adenoma with renal complications (distal RTA) brought out by prolonged hypercalcemia and medullary nephrocalcinosis [Figure 2]. The patient’s hypercalcemia was only managed with intravenous hydration and increased oral fluid intake. Patient was advised for surgical removal of adenoma.
Figure 1: Parathyroid scan with Tc 99 M Sestamibi shows abnormal focal tracer uptake (arrow) below the left lobe of thyroid gland suggestive of left inferior parathyroid adenoma.

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Figure 2: Mechanism of renal tubular acidosis in primary hyperparathyroidism.

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   Discussion Top


Medullary nephrocalcinosis is one of the clinical presentations of primary hyperparathyroidism.[5] Alkaline urine along with hypercalciuria are risk factors for medullary nephrocalcinosis. Hypercalciuria and parathyroid hormone excess, or the presence of both of these mechanisms may cause damage to renal tubular epithelium. This tubular damage leads to defective urinary acidification process.[6] Proximal tubular function is usually commonly affected in hyperparathyroidism, but longer disease duration may give rise to medullary nephrocalcinosis and in turn distal RTA. Around 10% to 20% of cases of hypercalciuric nephrolithiasis are associated with distal RTA.[7] Muthukrishnan et al, reported distal RTA (normal anion gap metabolic acidosis with urine pH >5.5, a positive urine anion gap, and a positive ammonium chloride loading test) in four of the 53 patients with symptomatic PHPT.[4] On the basis of reversibility of the distal RTA (after surgical treatment of PHPT), the authors hypothesized PHPT as the primary cause of distal RTA in these cases.[4]

On the contrary, primary hyperparathyroidism results in proximal RTA and hypophosphatemia secondary to inhibition of Na/H exchange and sodium-phosphate cotransport in the proximal tubule. The parathyroid hormone inhibits proximal tubular bicarbonate reabsorption, which tends to cause mild metabolic acidosis (proximal tubular acidosis). However, this effect is usually counterbalanced by the alkali liberated as a result of increased bone resorption and tubular reabsorption of the bicarbonate, caused by hypercalcemia.[8]

Parathyroidectomy often leads to a reduction of stone recurrence rates although formed stones may be present.[9] Parathyroidectomy can cause complete resolution of distal RTA as was shown by Muthukrishnan et al.[4] Our patient was advised to undergo parathyroidectectomy. Patient till then was managed with high fluid intake along with crystallization inhibitors like citrate. Citrate is metabolized in the liver to bicarbonate, which results in urinary alkalization and therefore reduced citrate reabsorption in the renal tubule. This urinary citrate then binds to calcium and forms a soluble complex, thus reducing the precipitation of calcium salt in the renal tubule. Urinary calcium excretion has been found to be reduced by up to 30% with adequate alkali citrate treatment, thus has been shown to decrease progression of nephrocalcinosis.[10]


   Conclusion Top


PHPT may present initially as electrolyte imbalance like hypokalemia secondary to RTA. Even if kidney dysfunction persists for more than three months, one should look at reversible causes, especially if the presentation is with normal kidney size and electrolyte imbalance. In our case, patient on initial evaluation was wrongly labeled as chronic kidney disease with secondary hyperparathyroidism, but strong clinical suspicion with further evaluation for hypokalemia lead us to a diagnosis of distal RTA secondary to medullary nephrocalcinosis due to primary parathyroid adenoma-induced hypercalcemia. Thus hyperparathyroidism should be kept as a differential, especially in young patients who presents with significant electrolyte imbalance.

Conflicts of interest: None declared.

 
   References Top

1.
Peacock M. Primary hyperparathyroidism and the kidney: Biochemical and clinical spectrum. J Bone Miner Res 2002;17 Suppl 2:N87-94.  Back to cited text no. 1
    
2.
Siddiqui AA, Wilson DR. Primary hyperparathyroidism and proximal renal tubular acidosis: Report of two cases. Can Med Assoc J 1972; 106:654-9.  Back to cited text no. 2
    
3.
Buckalew VM Jr. Nephrolithiasis in renal tubular acidosis. J Urol 1989;141:731-7.  Back to cited text no. 3
    
4.
Muthukrishnan J, Hari Kumar KV, Jha R, Jha S, Modi KD. Distal renal tubular acidosis due to primary hyperparathyroidism. Endocr Pract 2008;14:1133-6.  Back to cited text no. 4
    
5.
Keating FR Jr. Diagnosis of primary hyperparathyroidism. Clinical and laboratory aspects. JAMA 1961;178:547-55.  Back to cited text no. 5
    
6.
Hulter HN, Peterson JC. Acid-base homeostasis during chronic PTH excess in humans. Kidney Int 1985;28:187-92.  Back to cited text no. 6
    
7.
Arruda JA, Cowell G. Clinical disorders of acid-base physiology. Curr Nephrol 1989;12: 39-79.  Back to cited text no. 7
    
8.
Lila AR, Sarathi V, Jagtap V, Bandgar T, Menon PS, Shah NS. Renal manifestations of primary hyperparathyroidism. Indian J Endocrinol Metab 2012;16:258-62.  Back to cited text no. 8
    
9.
Peacock M, Robertson WG, Marshall RW. Disorders associated with recurrent calcium containing kidney stones. In: De Groot LJ, Cahill GF, Martini L, editors. Endocrinology 2. New York, NY, USA: Grune & Stratton; 1979. p. 823-37.  Back to cited text no. 9
    
10.
Habbig S, Beck BB, Hoppe B. Nephrocalcinosis and urolithiasis in children. Kidney Int 2011;80:1278-91.  Back to cited text no. 10
    

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Correspondence Address:
Dr. Manish R Balwani
Department of Nephrology, Jawaharlal Nehru Medical College, Sawangi, Wardha - 442 001, Maharashtra
India
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DOI: 10.4103/1319-2442.243965

PMID: 30381523

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    Abstract
   Introduction
   Case Report
   Discussion
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