Lumbar Tuberculosis Associated with Membranous Nephropathy and Interstitial Nephritis

Abstract

Tuberculosis is a common disease worldwide. However, it now is clear that tuberculosis can affect the kidney more insidiously. We describe a case of lumbar tuberculosis associated with simultaneous membranous nephropathy and interstitial nephritis, in which recovery of renal function occurred after treatment with steroids in addition to antituberculosis agents. CASE REPORTA 50-year-old woman was admitted to the hospital with a 2-week history of hematuria, proteinuria, and renal failure. She had been diagnosed with lumbar tuberculosis (TB) 6 weeks earlier because of mild fever, fatigue, night sweating, weight loss, and low-back pain. Her tuberculin skin test was strongly positive. A colloidal-gold-based serological assay with a Mycobacterium tuberculosis antibody assay kit (Assure TB Rapid Test; MP Biomedicals Asia Pacific Pte. Ltd., Singapore) was used to detect M. tuberculosis antibody. The result was positive. Lumbar X-ray examination showed that the L3-L4 disc space was narrow and destroyed ( Fig. 1). She had been treated with rifampin, isoniazid, ethambutol, and pyrazinamide for 4 weeks before admission. Her temperature normalized, and the lowback pain disappeared. However, 2 weeks before the admission, she developed hematuria and proteinuria. Her serum creatinine, which had been 63 mol/liter 1 month prior to presentation, rose to 183 mol/liter. She reported no abnormal urinary frequency, dysuria, or flank pain. Her remaining medical history, travel history, and family history were unremarkable. Physical examination showed a body temperature of 36.8°C, a regular pulse rate of 85/min, respiratory rate of 18/ min, and blood pressure of 140/85 mm Hg. Laboratory findings included a hemoglobin level of 9.3 g/dl, a platelet count of 320 ϫ 10 9 /liter, and a white cell count of 11.7 ϫ 10 9 /liter. The erythrocyte sedimentation rate was 24 mm/h, and C-reactive protein was 5.45 mg/dl. The blood urea nitrogen was 7.34 mmol/liter, and serum creatinine was 183 mol/liter. Serum complement levels were normal. Urinalysis revealed 2ϩ protein, with 12 to 15 red blood cells and 16 to 20 white blood cells per high-power field (HPF) in the urinary sediment. Daily urinary protein excretion was 2.6 g. Complement 3 (C3) and C4 concentrations were normal. Serology for antinuclear antibody, human immunodeficiency virus, and syphilis was negative, and the patient was not otherwise immunocompromised. Sputum smears for acid-fast stain were negative. Chest X-ray examination was normal. Renal ultrasonography showed normal-size kidneys without any abnormality. PCR analysis using specific primers for M. tuberculosis was performed on earlymorning urine samples for three consecutive days. DNA was extracted from the urine samples with the QIAamp DNA minikit (Qiagen, Hilden, Germany) according to the manufacturer's instructions. The primers targeted to the specific insertion element insertion sequence (IS) IS6110 of M. tuberculosis were synthesized by Takara Bio Inc. (Dalian, China). The amplicon size was 156 bp. The results were positive (Fig...

Membranous glomerulonephritis associated with Mycobacterium shimoidei pulmonary infection

“…In several cases with MGN due to M. tuberculosis , urinary protein excretion caused by MGN was improved by treatment with antituberculosis agents with or without prednisolone (30 mg/d) [ 17 , 18 ]. Some patients with tuberculosis present glomerular diseases other than MGN, including IgA nephropathy, focal proliferative glomerulonephritis, and focal segmental glomerulosclerosis [ 21 – 24 ].…”

“…Regarding the mechanisms by which tuberculosis causes glomerular diseases, immune responses may be involved. M. tuberculosis was reported to induce both cellular and humoral immune responses when the bacilli invade the body [ 17 ]. M. tuberculosis infection can lead to disturbance of Th1/Th2 cells, which may give rise to nephritis [ 25 ].…”

“…Several cases with MGN due to M. tuberculosis have also been reported without classical renal tuberculosis [17,18]. However, there are no reports describing MGN caused by non-tuberculous mycobacterium (NTM) infection.…”

“…It is well-known that membranous glomerulonephritis (MGN) can occur secondarily from malignancy, drugs and toxic substances, collagen diseases such as systemic lupus erythematosus, and infectious diseases, including hepatitis B, quartan malaria, and schistosomiasis [ 16 ]. Several cases with MGN due to M. tuberculosis have also been reported without classical renal tuberculosis [ 17 , 18 ]. However, there are no reports describing MGN caused by non-tuberculous mycobacterium (NTM) infection.…”

An Implication of Relationship between Tuberculosis and Primary Nephrotic Syndrome

“…There have been few case reports on the concurrence of PNS and TB. In some cases symptoms of PNS were relieved after anti-tubercular therapy alone (5–9). The phenomenon implicated an etiological relationship between TB and PNS.…”