IgA glomerulonephritis may present with gross hematuria and flank pain [
A 25-year-old female with no prior medical history presented to the emergency department due to high fever (up to 39°C) since 3 days. She complained of left flank pain and gross hematuria. On physical examination, left costovertebral angle tenderness was noted. The urinalysis confirmed the hematuria (2055 red blood cells per high-power field). The urinary dipstick was negative for leukocyte esterase and for nitrites, but significantly positive for albuminuria (2+). On microscopic examination of the urine, pyuria was minimal (6 white blood cells per high-power field) and no bacteriuria was noted. She denied having taken antibiotics before presentation. Urine and blood cultures were obtained. The laboratory tests revealed a significantly elevated C-reactive protein (CRP = 28 mg/dl), a high erythrocyte sedimentation rate (107 mm/h), and an elevated creatinine (1.21 mg/dl) with normal blood urea nitrogen (16 mg/dl).
She was admitted to the internal medicine ward with a preliminary diagnosis of acute pyelonephritis, and she was started on intravenous ceftriaxone. A contrast-enhanced computed tomography the next day revealed a hypoenhancing region in the upper pole of the left kidney, suggestive of pyelonephritis (Figure
Contrast-enhanced computed tomography demonstrating a hypoenhancing region in the left kidney.
A biopsy of the left kidney was performed at the 6th day of hospital stay and confirmed a diagnosis of IgA nephropathy (immunofluorescence was strongly positive for mesangial IgA deposition, complement component C3, and lambda light chains and moderately positive for IgM). The patient denied any recent respiratory tract infection symptoms. Other lab tests sent during her hospital stay were normal (lactate dehydrogenase, anti-neutrophil cytoplasmic antibodies, antinuclear antibodies, anticardiolipin IgG and IgM, anti-beta-2 glycoprotein I IgG and IgM, protein electrophoresis, serum complement C3c and C4 level, rheumatoid factor, and transesophageal echocardiography). She was started on lisinopril 5 mg daily. Furthermore, considering the significant proteinuria, the elevated creatinine and the negative prognostic features of the biopsy, (M1E1S1T0C1 according to the Oxford classification [
Despite a clinical presentation typical for pyelonephritis (high fever, flank pain, and costovertebral angle tenderness) and compatible imaging (computed tomography) and laboratory tests (high CRP), our patient was diagnosed with IgA nephropathy, confirmed by kidney biopsy. The lack of pyuria, the negative dipstick for nitrites and leukocyte esterase, and the fact that both urine and blood cultures were negative, despite both being obtained before initiation of antimicrobial therapy, put in doubt the diagnosis of pyelonephritis. Nevertheless, the negative predictive value of urinalysis may be lower [
Possible reasons for culture-negative pyelonephritis include antibiotic pretreatment, difficult to culture atypical microorganisms such as
The presence of significant proteinuria was another important clue for reaching the correct diagnosis in our patient. Transient low-level proteinuria can also occur due to fever or urinary tract infection [
The very high CRP in our case is an unexpected finding for IgA nephropathy in the absence of infection, since such high elevations have not been described in prior studies [
The imaging on computed tomography in our patient is also unusual for IgA nephropathy. However, focal hypoenhancing areas on computed tomography in the setting of IgA nephropathy have been described by other authors too [
Of note is that our patient reported a similar prior episode in the past (fever accompanied by hematuria) at which time she had been treated with antibiotics, and no further work-up was performed. Although it is unclear if that episode represented the first manifestation of IgA nephropathy, confirming the diagnosis of IgA nephropathy at that time could have prevented long-term kidney damage.
In conclusion, even in cases with clinical presentation typical for pyelonephritis, gross hematuria should raise the suspicion for underlying IgA nephropathy, especially in the absence of pyuria or bacteriuria and when there is acute worsening of renal function. In such cases, it is reasonable to perform a microscopic examination of the urinary sediment looking for signs of glomerular disease (especially red blood cell casts and dysmorphic red blood cells). Misdiagnosing IgA nephropathy-associated episodes of hematuria as urinary tract infections may lead to long-term irreversible kidney damage.
The authors declare that they have no conflicts of interest.