This is a fascinating case, witnessed by Mandal etal., of a patient complaining of isolated gross hematuria with unremarkable clinical signs and symptoms. It is essential to differentiate between glomerular and non-glomerular hematuria for making appropriate clinical decisions. Glomerular hematuria is identied by the presence of red blood cell casts, dysmorphic red cells, and albuminuria (500mg/24h). Acanthocytes, also called spur cells, are irregularly shaped red cells with vesicle­like protrusions. Acanthocytes become a highly specic (98%) indicator for glo­merular disease if their numbers exceed 5% on phase-contrast microscopy [10]. Though this criterion is relevant clinically, its absence does not entirely rule out the possibility of glomerular disease. IgA nephropathy, Alport syndrome, and thin base­ment membrane disease are the three signicant disorders in patients who present with isolated macrohematuria [2]. Upon examination, this patient denied any recent history of infections and had normal visual acuity and hearing. The diagnosis gravi­tated toward C1q nephropathy due to the presence of C1q deposits within the mesangium and a few of them in the subendothelial region. C1q nephropathy was rst chronicled in the year 1985 by Jennette and Hipp. The denition is histological, with characteristic C1q deposits in the renal mesangium in a dominant or codomi­nant fashion and the absence of clinical features indicative of systemic lupus erythe­matosus (SLE) and membranoproliferative glomerulonephritis (MPGN) [4, 7]. The serological markers show negative antinuclear antibodies and normal complement levels [11]. One of the studies done by Vizjak etal. clearly emphasized the rarity of C1q nephropathy among healthy individuals. C1q immune deposits were com­monly seen in patients having tubulointerstitial nephritis, proven hypertensive neph­rosclerosis, thin basement membrane nephropathy, and hantavirus nephropathy. Markowitz et al. described C1q deposits as a nonspecic marker of increased mesangial trafcking in the setting of glomerular proteinuria [6, 12]. The pathogen­esis of C1q nephropathy lacks clarity, and due to the avid use of C1q staining, the benign positive rates are escalating. This portrays a particular bias leaving potential differentials under the shadow [7]. This patient had a slight exception where C1q deposits were observed in a healthy individual with no history of preexisting renal condition and no family history of renal abnormalities. One of the key tests that pointed against the glomerular cause of hematuria was urine light microscopy, where the erythrocytes were normal appearing without any casts or dysmorphic features.