Keyword: Case Report

ABSTRACT: Background: IgA nephropathy (IgAN) is an immune complex–mediated glomerular disease characterized by marked clinical and histopathological heterogeneity and a variable risk of progression. The coexistence of IgAN with features of TMA poses a particular diagnostic challenge, as a microangiopathic phenotype may emerge in the setting of severe glomerular injury, endothelial dysfunction, complement activation, and additional external triggers. The clinical consequences of such an interaction may be particularly significant in patients with a solitary functioning kidney.
Objective: To characterize the clinicopathological features of severe IgAN presenting with a clinical–hematological TMA phenotype in a young woman with a solitary functioning kidney and to explore the potential contribution of local complement activation and recurrent drug exposures as a putative “second hit” to endothelial injury and rapid deterioration of kidney function.
Case presentation: A 22-year-old woman had a solitary functioning right kidney following neonatal left nephrectomy. Kidney function remained preserved for years; however, persistent microscopic hematuria had been documented since 2022, retrospectively suggesting clinically silent glomerular disease. Between 2022 and 2026, she had substantial cumulative exposure to medications and supplements, including recurrent antiviral, antibacterial, and anti-inflammatory therapies, acne-directed treatments, vitamin/mineral preparations, and dietary supplements. These exposures preceded clinical deterioration and were considered potential external triggers in a susceptible renal background rather than evidence of definite drug-induced TMA. In June–July 2026, she developed recurrent massive edema followed by rapidly progressive kidney dysfunction with azotemia, hyperkalemia, active urinary sediment, and proteinuria, ultimately requiring hemodialysis. During hospitalization, microangiopathic hemolytic anemia, severe thrombocytopenia, schistocytosis, reticulocytosis, and elevated lactate dehydrogenase established a clinical–hematological TMA phenotype (Table 1). Preserved ADAMTS13 activity argued against immune-mediated thrombotic thrombocytopenic purpura (TTP), while autoimmune, anti-GBM, antiphospholipid, and infectious investigations were unrevealing. Given rapidly progressive dysfunction of the solitary kidney and an active nephritic syndrome, methylprednisolone and cyclophosphamide were administered before histopathological confirmation. Two sessions of therapeutic plasma exchange were subsequently performed in the setting of the pronounced TMA phenotype. Hematological parameters improved, whereas kidney function did not recover and dialysis dependence persisted. Kidney biopsy demonstrated advanced IgAN with severe chronic kidney damage (Oxford Classification M0E1S1T2C1) and intense mesangial IgA/C3 codeposition despite normal circulating C3. No definitive histopathological evidence of active TMA was identified.
Conclusion: This case demonstrates previously oligosymptomatic IgAN presenting with rapidly progressive kidney dysfunction, dialysis-dependent kidney failure, and a compelling clinical–hematological TMA phenotype. Preserved ADAMTS13 activity and an unrevealing investigation for major secondary causes supported a microangiopathic process distinct from immune-mediated TTP. Marked mesangial IgA/C3 codeposition despite normal circulating C3 raises the possibility that local complement activation may have amplified glomerular inflammation and endothelial injury. However, these findings are insufficient to establish complement-mediated TMA. The absence of active TMA lesions in a biopsy obtained later in the disease course likewise does not establish renal TMA, but cannot exclude a preceding transient or partially resolved microangiopathic process.  A distinctive feature was the substantial cumulative medication and supplement exposure preceding clinical deterioration. In the setting of pre-existing IgAN and a solitary functioning kidney, recurrent drug exposures may have constituted an external “second hit,” potentially promoting immune activation, endothelial stress, and clinical decompensation. The absence of a clear temporal relationship with a single agent, however, precludes attribution to definite drug-induced TMA. Collectively, this case supports a multifactorial, hypothesis-generating model: pre-existing IgAN in a solitary kidney → recurrent external/drug exposures as a potential “second hit” → possible local complement activation and endothelial injury → clinical–hematological TMA phenotype → rapid kidney function deterioration. This proposed sequence should not be interpreted as evidence of direct causality.
Clinical lesson: in patients with IgAN and rapidly deteriorating kidney function, particularly when anemia and thrombocytopenia develop, targeted evaluation for TMA and potential secondary triggers should be considered even when circulating C3 levels are normal.

ABSTRACT: Patient T., 43 years old. End-stage chronic kidney disease (CKD) was diagnosed in 2013, and emergency kidney replacement therapy with maintenance hemodialysis was initiated. Prior to this, the patient had not been followed by a nephrologist. Throughout the course of hemodialysis treatment, the patient failed to comply with medical recommendations regarding regular laboratory monitoring of mineral metabolism.
In 2024, a markedly elevated parathyroid hormone (PTH) level (>1,935 pg/mL; October 2024) was detected for the first time. The patient had not received any specific medical therapy. Clinical manifestations included generalized weakness, bone and joint pain, impaired mobility (waddling gait), and skeletal deformities involving the sternum and tibial bones.
Scintigraphy performed on December 13, 2024, demonstrated increased functional activity of all four parathyroid glands (Figure 1). Despite prolonged combined medical therapy with cinacalcet 90 mg/day and paricalcitol 15 μg three times weekly, laboratory markers of calcium-phosphate metabolism continued to deteriorate, with the PTH level rising to 2,338 pg/mL. Bone mineral density assessment by dual-energy X-ray absorptiometry (DXA) revealed a Z-score of −5, consistent with severe secondary osteoporosis (Figure 2).
In December 2024, the patient underwent cervical exploration with removal of the hyperplastic left superior, left inferior, and right inferior parathyroid glands at Poytaxt Medical Clinic. In the postoperative period, a significant reduction in serum PTH was observed, decreasing to 492 pg/mL (December 27, 2024) compared with the preoperative level of 2,338 pg/mL.
During the one-year follow-up after parathyroidectomy, the patient's condition remained stable, with no recurrence of hyperparathyroidism. As replacement therapy, the patient has been receiving long-term calcium supplementation and alfacalcidol.
Biochemical blood tests performed in August–September 2025 demonstrated total serum calcium levels ranging from 1.79 to 2.71 mmol/L (reference range: 2.1–2.6 mmol/L) and serum phosphorus levels of 1.0–1.15 mmol/L (reference range: 0.81–1.45 mmol/L).
In November 2025, dysfunction of the patient's arteriovenous fistula (AVF) resulted in complete loss of vascular access. The exact etiology could not be established because of insufficient diagnostic evaluation; however, vascular wall calcification was considered a possible contributing factor. A temporary central venous catheter was inserted for hemodialysis, followed by successful creation of a new arteriovenous fistula.
According to the most recent laboratory evaluation performed on January 7, 2026, the PTH level remained within the target range (200 pg/mL), serum phosphorus was 0.98 mmol/L, and alkaline phosphatase was 410.5 U/L.
Conclusion: This clinical case illustrates the consequences of delayed diagnosis and inadequate management of secondary hyperparathyroidism, resulting from both poor patient adherence to treatment and systemic healthcare limitations, including insufficient long-term follow-up, limited access to regular laboratory monitoring, and shortcomings in the standard management of maintenance hemodialysis patients.
Although parathyroidectomy is effective in improving quality of life and reducing cardiovascular mortality, it is associated with postoperative complications and is generally performed only in advanced stages of the disease, when irreversible disorders of mineral and bone metabolism have already developed.
Therefore, early diagnosis and timely initiation of long-term medical therapy remain the cornerstone of secondary hyperparathyroidism management, allowing better disease control and reducing the need for surgical intervention.

ABSTRACT: Post-bariatric surgery patients face higher risk of micronutrient malabsorption and often receive intravenous iron like Ferric carboxymaltose (FCM).  Recent studies associate FCM with severe (serum phosphate levels < 1 mg/dL) and prolonged hypophosphatemia caused by elevated Fibroblast Growth Factor 23 (FGF23) levels, which reduces phosphate reabsorption in the kidneys via α-Klotho co-receptor. FCM, in particular, can therefore lead to notable and sustained FGF23-mediated hypophos-phatemia. We present a case of prolonged and severe hypophosphatemia secondary to fibroblast growth factor 23 (FGF23)-mediated phosphaturia following ferric carboxymaltose (FCM) administration in a post-bariatric surgery patient. This case underscores the complex interplay between intravenous iron therapy, phosphate metabolism, and altered absorption physiology following bariatric surgery. It highlights the need for clinicians to monitor phosphate levels after FCM administration, particularly in high-risk patients such as those with malabsorption.

ABSTRACT: A 41-year old female patient who underwent kidney transplantation as an outcome of chronic glomerulonephritis came to the hospital with the signs of acute upper respiratory tract infection. As the patient further developed oliguria, peripheral edema, fever, and an increased BP, she was further relocated to the University Medical Center (UMC). Upon admission to UMC, signs of septic shock were detected, and acute transplant rejection was suspected, to exclude which kidney biopsy was performed and stage 3 chronic kidney disease (CKD) in allograft kidney was detected. Antibacterial treatment as well as pulse therapy were performed as patient had septic shock and tubulointerstitial nephritis (TIN).

ABSTRACT: A 46-year old male was admitted to the University Medical Center (UMC) hospital with the following symptoms of anuria, abdominal fullness, hypotension, exertional dyspnea, and peripheral edema. The purpose of his visit was the insertion of a peritoneal dialysis catheter. He had chronic kidney disease stage 5 as a consequence of diabetic nephropathy, liver cirrhosis due to hepatitis C infection, and HIV. His disease course was further complicated by the presence of a urinary tract infection. As a result of his multiple comorbidities, he underwent a complex treatment regimen which included renal replacement therapy with ultrafiltration, blood transfusions for his anemia, platelet transfusions for his thrombocytopenia, albumin infusion for his hypoalbuminemia, and antibiotic treatment for his concurrent infection. Additionally, he received diuretic treatment for his hypervolemia and anti-hypertensives to control his blood pressure. After peritoneal dialysis (PD) insertion, the patient successfully underwent PD and was discharged home.