Tonsillitis to Tubules: Unravelling the Cause of Acute Kidney Injury
Anjam Nassar, Dr. Himanshu Gul Mirani, Rakan Khalifa
Case Presentation:
A previously well young adult presented to the Emergency Department (ED) with acute onset of systemic illness marked by dysuria, oliguria, flank pain, and generalized body aches. The clinical picture evolved following a sore throat and urinary tract infection (UTI) treated with antibiotics, with subsequent development of a rash and reduced oral intake. The combination of systemic symptoms, rash, and rising creatinine suggested a possible acute kidney injury (AKI), prompting further diagnostic workup to explore potential causes including glomerulonephritis, interstitial nephritis, or pyelonephritis.
Case History:
The patient had experienced sore throat and UTI symptoms 10 days prior, treated initially with antibiotics by a general practitioner. Three days before presentation, their symptoms worsened, leading to a prescription for Penicillin V, which was stopped due to a rash. The patient reported vomiting, significant reduction in oral intake, and decreased urine output. On examination in the ED, they were febrile (37.3°C), tachycardic (HR 108), hypotensive (BP 98/64), and appeared clinically dehydrated. Examination revealed bilateral active tonsillitis, right flank tenderness, a blanching pruritic erythematous rash on the arms, but no peripheral oedema.
Management and Outcome:
Initial investigations showed severe renal impairment with urea 23 mmol/L, creatinine 568 µmol/L, and an eGFR of 8 mL/min/1.73m². Her previous renal function was normal. Arterial blood gas indicated high anion gap metabolic acidosis (HAGMA) with a pH of 7.26 and bicarbonate of 13 mmol/L. Inflammatory markers were elevated (CRP 281 mg/L, WCC 19 x10⁹/L), with normal platelets and no eosinophilia. Serum sodium and potassium were within normal range. Imaging (CT KUB and POCUS) revealed bilaterally swollen kidneys
with no hydronephrosis or renal calculi. A chest X-ray was unremarkable. Complement levels were normal, immunoglobulin panel including IgA was within normal range, and albumin creatinine ratio (ACR) was elevated at 60 mg/mmol.
IgA nephropathy (IgAN), also known as Berger’s disease, is characterized by mesangial deposition of IgA, often following mucosal infections like tonsillitis, and may present with hematuria and AKI (Wyatt & Julian, 2013, NEJM). IgAN affects around 1 in 50,000 people in the UK. It is one of the most common causes of chronic kidney disease and kidney failure (Kidney Care UK). IgAN develops within days of the onset of upper respiratory tract infection, while PSGN occurs after weeks.
PSGN typically follows streptococcal infections, presenting with nephritic syndrome, low complement levels, and elevated ASOT, though normal complement in this case makes it less likely (Tunkel et al., 2017, NEJM).
Drug-induced acute interstitial nephritis, particularly from beta-lactam antibiotics, is another plausible cause, typically manifesting with fever, rash, and renal impairment, and is often not accompanied by eosinophilia (Perazella, 2019, BMJ).
Key Learning Points:
The clinical scenario suggests an acute glomerular or interstitial renal process likely triggered by a preceding infection or drug reaction. Differential diagnoses include IgA nephropathy, post-streptococcal glomerulonephritis (PSGN), and drug-induced interstitial nephritis, particularly in light of recent penicillin exposure and allergic-type rash. Management included intravenous fluids, renal dose-adjusted ciprofloxacin, and sodium bicarbonate for metabolic acidosis. Upon follow up, the patient’s renal biopsy confirmed IgA nephropathy. The patient made complete recovery of her renal function by 2 months.