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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2001  |  Volume : 12  |  Issue : 4  |  Page : 534-537
A Case of Progressive Tubulo-Interstitial Nephritis due to Culture-negative Renal Tuberculosis


1 Department of Medicine, Faculty of Medicine, Kuwait University, Kuwait
2 Department of Pathology, Ministry of Health, Kuwait
3 Department of Medicine, Ministry of Health, Kuwait

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   Abstract 

This report describes a woman with progressive renal failure without proteinuria, urinary obstruction or overt systemic disease. The progressive renal disease without pelvicalyceal deformities in the left kidney was not consistent with the vesicoureteric reflux nephropathy. A needle biopsy of the left kidney showed interstitial caseating granulomata. The patient did not have clinical, radiological or urine culture evidence of renal tuberculosis. She improved after treatment with antituberculous therapy. This case report demonstrates the value of kidney biopsy in establishing the diagnosis of such common and treatable disease even if clinically silent and urine culture negative.

How to cite this article:
El-Reshaid KA, Madda JP, Al-Saleh MA. A Case of Progressive Tubulo-Interstitial Nephritis due to Culture-negative Renal Tuberculosis. Saudi J Kidney Dis Transpl 2001;12:534-7

How to cite this URL:
El-Reshaid KA, Madda JP, Al-Saleh MA. A Case of Progressive Tubulo-Interstitial Nephritis due to Culture-negative Renal Tuberculosis. Saudi J Kidney Dis Transpl [serial online] 2001 [cited 2019 Sep 16];12:534-7. Available from: http://www.sjkdt.org/text.asp?2001/12/4/534/33550

   Introduction Top


Tubulointerstitial nephritis (TIN) accounts for up to 30% of the cases of end-stage renal disease in Kuwait. [1] The disease can result, primarily, from exposure to various therapeutic or environmental agents or in association with a number of systemic illnesses or infections. [2] Early diagnosis and treatment can slow down the progression of the chronic disease or reverse the acute one. Most of the cases of TIN have been attributed to vesicoureteric reflux (VUR). However, progressive renal insufficiency associated with VUR occurs in two circumstances. In a large percentage of the cases, the disease is severe and affects both kidneys with coarse scar formation. The rest of the cases are due to progressive glomerulopathy that manifests with hyper­tension and proteinuria. [2]

In our case report, we describe a patient with progressive disease due to silent tuberculous infection and demonstrate the limitations of "non-invasive" testing in establishing the diagnosis.


   Case Report Top


A 44-year-old Kuwaiti woman was evaluated at Al-Amiri Hospital in Kuwait, for progressive renal failure. Her serum creatinine, which was 120 µmol/L six months prior to presentation rose to 160 µmol/L. She denied fever, weight loss, decreased appetite or cough. She had hypertension diagnosed seven years earlier, which was controlled with atenolol 100 mg daily and hypothyroidism due to Hashimoto's thyroiditis stabilized by L-thyroxin 100 µg daily. Review of the patient's medical reports showed that she had isolated hematuria in one of three urinalysis specimens in the past six months. The patient's family history revealed that one of her sisters and her son were treated for tuberculosis 10 years ago.

On examination she was slim, not in distress, afebrile and her blood pressure was 120/80 mm Hg. She did not have lymphadenopathy, goiter, skin rash, joint disease or edema. The rest of the physical examination was unremarkable.

The laboratory investigations showed normal peripheral leukocyte and platelet counts. Hemoglobin level was 120 g/L with MCV 81 fL. ESR was 41 mm/h. Serum glucose, sodium, potassium, calcium, CO2, bilirubin, alanine aminotransferase and alkaline phosphatase were within normal limits. Urinalysis was also within normal limits. The 24-hours urine collection revealed creatinine clearance of 48 ml/min and protein execration of 100 mg/day. Thyroid stimulating hormone was 3 mU/L.

Chest x-ray (posterio-anterior and lordotic views) was normal. Ultrasound examination of the abdomen and pelvis did not show any abnormality except for bilaterally echogenic kidneys. The right kidney was relatively small (9 cm) and with irregular outline. Intravenous pyelogram (IVU) showed small and poorly functioning right kidney with calicyectasis and normal left kidney [Figure - 1]. Computerized tomography (CT) scan of the chest and abdomen did not show any hilar or para-aortic lymphadenopathy.

However, basal lobe fibrosis was noted. Angiotensin converting enzyme level was normal. Early morning urine specimens on three consecutive days were negative for acid-fast bacilli using concentration methods and culture. Tuberculin skin test was positive 20 mm after 48 hours. Biopsy of the left kidney, showed focal areas of segmental interstitial fibrosis and mononuclear cell infiltration associated with caseating granu­lomata [Figure - 2]. Glomerular architecture was preserved and blood vessels showed mild hypertensive changes. Immunofluo­rescent staining was negative for immuno­globulin deposits. The patient was treated for probable renal tuberculosis with rifampicin, INH, pyrazinamide, ethambutol and pyridoxine for six months. Serum creatinine decreased to 102 µmol/L four months later and 80 µmol/L on completion of treatment.


   Discussion Top


The patient in this case report did not have clinical manifestations or laboratory evidence of active tuberculosis and her kidney disease could have been labeled as "chronic pyelonephritis due to reflux nephropathy". There was a progressive deterioration of kidney function below 50 ml/min in the left kidney did not show significant pelvi­calyceal changes on IVU examination. Furthermore, there was a proteinuria or severe hypertension. These findings were not consistent with a reflux disease. [3]

Despite the risks of performing percutaneous biopsy of a relatively single functioning kidney, [4] we elected to perform it to investigate the etiology of the patient's active renal disease. This approach helped to diagnose her disease since, three urine cultures which is considered "the gold standard for diagnosis of renal tuberculosis", [5] failed to show any acid-fast bacilli.

Previous studies have shown that the natural history of renal tuberculosis starts with granulomatous lesions in the glomeruli during the primary infection, which often heal or rupture, (sometimes as late as after 30 years), into a) the interstitium leading to interstitial fibrosis or b) tubules leading to strictures. [6] Since the rupture of glomerular granulomata is a random event independent of any active tuberculosis elsewhere, it is rarely associated with systemic symptoms or pulmonary disease. [7] Moreover, the periodic rupture into the interstitium tubules can be associated with disease primarily in the interstitium without persistent pyuria, hematuria or identifiable AFB in urine testing including short-term culture studies as in our case. [8]

This case report demonstrates the value of kidney biopsy in patients with tubulo­interstitial nephropathy due to tuberculosis in the absence of radiological and urine findings.

 
   References Top

1.El-Reshaid K, Johny KV, Sugathan TN, Hakim A, Georgous M, Nampoory MR. End-stage renal disease and renal replacement therapy in Kuwait: epidemiological profile over the past 4½ years. Nephrol Dial Transplant 1994;9:532-8.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Kelly CJ, Neilson EG. Tubulointerstitial disease. In: Brenner BM (ed). The kidney. Philadelphia, USA, W.B. Saunders Press 1996;1655-79.  Back to cited text no. 2    
3.Arant BS Jr. Vesicoureteric reflux and renal injury. Am J kidney Dis 1991;17:491-511.  Back to cited text no. 3    
4.Parrish AE. Complications of percutaneous renal biopsy: a review of 37 years experience. Clin Nephrol 1992;38:135-41.  Back to cited text no. 4  [PUBMED]  
5.Diagnostic standards and classification of tuber­culosis in adults and children. Am J Respir Crit Care Med 2000;161:1376-95.  Back to cited text no. 5    
6.Christensen WI. Genitourinary tuberculosis: review of 102 cases. Medicine Baltimore 1974; 53:377-90.  Back to cited text no. 6  [PUBMED]  
7.Simon HB, Weinstein AJ, Pastermak MS, Swartz MN, Kunz LJ. Genitourinary tuber­culosis. Clinical features in a general hospital population. Am J Med 1977;63:410-20.  Back to cited text no. 7    
8.Lattimer JK, Reilly RJ, Segawa A. The signifi­cance of the isolated positive urine culture in genitourinary tuberculosis. J Urol 1969;102:610-3.  Back to cited text no. 8  [PUBMED]  

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Correspondence Address:
Kamel A El-Reshaid
Department of Medicine, Faculty of Medicine, Kuwait University, P.O. Box 24923, 13110 Safat
Kuwait
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PMID: 18209399

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    Abstract
    Introduction
    Case Report
    Discussion
    References
    Article Figures
 

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