Background: Although hypercalcemia typically causes renal dysfunction, our limited clinical experience suggests that renal impairment may be less common in patients with acquired hypocalciuric hypercalcemia (AHH), a calcium-sensing receptor (CaSR) autoantibody-mediated disorder. Aims: We evaluated whether AHH-induced severe hypercalcemia is less likely to impair renal function than parathyroid hormone-related peptide (PTHrP)-related hypercalcemia. Methods: The AHH group comprised eight cases: six literature cases, including five from our reports, and two new cases with albumin-corrected calcium (cCa) ≥13.5 mg/dL and available creatinine data. Controls were 29 patients with PTHrP-related hypercalcemia treated at our institution from 2015 to 2025. Age, sex, cCa, and estimated glomerular filtration rate (eGFR) were analyzed using adjusted linear regression and group-stratified models. Results: After adjustment for age and sex, eGFR was significantly better preserved in AHH than in PTHrP-related hypercalcemia. The interaction between group and cCa was significant (p for interaction=0.006), indicating different cCa-eGFR relationships. In stratified analyses, cCa showed a nonsignificant positive slope in AHH, whereas PTHrP-related hypercalcemia showed a significant negative slope (β=−12.5, p=0.0006). Conclusions: These findings suggest that AHH may be associated with reduced arginine vasopressin resistance, thereby protecting against dehydration and renal dysfunction despite marked hypercalcemia. The major outcome of the study is that preserved renal function despite severe PTH-dependent hypercalcemia may be an important clinical clue to AHH and should prompt evaluation for CaSR autoantibody-related disease.