Year : 2017 | Volume
: 28 | Issue : 1 | Page : 178--180
Typhoid-associated acute kidney injury masquerading as a relapse of Takayasu arteritis
Revanasiddappa Manjunath, Anupama Kaul, Raj Kumar Sharma, Dharmendra Singh Bhadauria, Narayan Prasad, Amit Gupta
Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
Renal dysfunction is common in Takayasu arteritis. Uncommonly, renal failure in a case of Takayasu arteritis can be due to an unrelated disease, and if the disease is a rare complication, it is even more difficult to diagnose. We report a 21-year-old male with type IV Takayasu arteritis presenting with fever and renal failure, who was diagnosed to have enteric fever- related glomerulonephritis which was successfully treated.
|How to cite this article:|
Manjunath R, Kaul A, Sharma RK, Bhadauria DS, Prasad N, Gupta A. Typhoid-associated acute kidney injury masquerading as a relapse of Takayasu arteritis.Saudi J Kidney Dis Transpl 2017;28:178-180
|How to cite this URL:|
Manjunath R, Kaul A, Sharma RK, Bhadauria DS, Prasad N, Gupta A. Typhoid-associated acute kidney injury masquerading as a relapse of Takayasu arteritis. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2021 Jan 27 ];28:178-180
Available from: https://www.sjkdt.org/text.asp?2017/28/1/178/198270
Takayasu arteritis is one of the common varieties of vasculitis seen in South Asian population. It is known to have relapsing- remitting course. Kidneys are one of the major organs involved. Renal failure in Takayasu arteritis can be prevented if the systemic disease is appropriately treated. However, the renal dysfunction in a patient with known Takayasu arteritis can be due to various causes, necessitating case-specific evaluation. We report a case of Takayasu arteritis with renal dysfunction.
A 22-year-old male presented to our follow-up clinic with history of fever, generalized myalgia, and headache for 10 days, decreased urine output, edema, and smoky urine for three days. His medical history included hypertension since the age of 19 years. He was evaluated for hypertension at our hospital and was diagnosed to be secondary to type IV Takayasu arteritis. He was started on prednisolone 1 mg/kg/day. He was lost to follow-up for two months, only to present later on with accelerated hypertension, right contracted kidney, and renal dysfunction (serum creatinine 281.6 μmol/L). He was managed with antihypertensive medications and prednisolone. Eventually, serum creatinine settled at 96.8 μmol/L. In view of uncontrolled hypertension and solitary functioning kidney, angioplasty of the left renal artery was done without any success. After the control of the disease activity, he underwent renal artery stenting with Formula™ (Cook Medical, Bloomington, IN). Hypertension was controlled on three drugs, with antihypertensive dose decreased by 50%; steroid was gradually tapered and stopped. On his last follow-up visit, three months before this presentation, he was off prednisolone, had well-controlled blood pressure on ramipril and furosemide. His renal function, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were normal.
Clinical examination showed pedal edema, heart rate of 68 beats/min, and temperature of 103°F. Blood pressure was 170/90 mm Hg. The rest of the clinical examination was unremarkable. Relevant investigations were sent. He was started on ceftriaxone 2 g/day and symptomatic medications. Investigations revealed total leukocyte count of 3.8 × 10/L, renal dysfunction (serum creatinine 369.6 μmol/L), high serum C3 (1.56 g/L), and C4 (0.49 g/L). He had a CRP of 5.6 mg/L and ESR of 51 mm/h. Urine analysis showed microscopic hematuria (35-40 red blood cells/high-power field and proteinuria (2+). Spot urine analysis showed a protein creatinine ratio of 1.87. On day 6, his leukopenia recovered, s. creatinine decreased to 167.2
μmol/L. His blood culture grew Salmonella typhi, sensitive to ceftriaxone, and ciprofloxacin. The ongoing treatment with ceftriaxone was continued. After eight days of antibiotics, he became afebrile. He was discharged on day 16 with stable renal function (serum creatinine 114.4 μmol/L), microscopic hematuria, and proteinuria.
On follow-up, it was noted that his antihypertensive dose was decreased, hematuria recovered by 5th month, proteinuria recovered by 7th month. At his last follow-up, he had a wellcontrolled blood pressure on ramipril and furosemide, with serum creatinine 96.8 μmol/L, the baseline value for this patient and an unremarkable urine analysis.
Takayasu arteritis commonly involves kidneys. It has a relapsing-remitting course. However, relapse may be misdiagnosed if not carefully interpreted. In our case, presentation with fever, hypertension, renal dysfunction, and raised ESR could have misled to a diagnosis of a relapse. The presence of microscopic hematuria and proteinuria, which is unusual for a case of Takayasu arteritis relapse, alerted us for an alternative diagnosis. Hence, steroids were withheld. In view of hypertension associated with high-grade fever, smoky urine, microscopic hematuria, and proteinuria, infectionrelated glomerulonephritis was considered. The blood culture taken at presentation was later reported to have grown S. typhi. Isolation of S. typhi from blood, bone marrow, is required for the definitive diagnosis of enteric fever. Blood culture has a sensitivity of 40-80%; bone marrow culture is 55-90% sensitive, and not affected by prior antibiotic therapy up to five days.
In our case, kidney biopsy was not done in view of the solitary functioning kidney. However, the presentation, laboratory evaluation, and the response to therapy with recovery of renal function, all support our diagnosis of infection-related glomerulonephritis or acute interstitial nephritis.
The diagnosis of enteric fever in endemic areas is easier when it presents with classical features. However, when it is an unusual presentation with a rare complication, it carries a risk of delaying the diagnosis and mistreating. Glomerulonephritis, acute interstitial nephritis, , pyelonephritis, and cystitis are rarely reported urinary complications of enteric fever. Other renal pathology reported with enteric fever is acute tubular necrosis, IgA Nephropathy, hemolytic-uremic syndrome, Henoch-Schφnlein purpura. , , , The incidence of these complications has decreased in view of prompt antibiotic treatment. Literature review reveals typhoid fever to be occasionally reported to cause glomerulonephritis, varying from asymptomatic urinary abnormality to acute renal failure. Overt glomerulonephritis is noted in about 2% of cases of acute enteric fever. However as many as 25% of these patients can have micros copic hematuria and proteinuria. Most of these reports are from developing countries, decades ago. With globalization and re-worsening of sanitary conditions, epidemic episodes of enteric fever are still reported.
Enteric fever-related GN and acute interstitial nephritis may be underdiagnosed (misinterpretation of reports/empirical treatment concealing the disease) or underreported. , ,
Conflict of interest: None declared.
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