Chronic kidney disease (CKD) is a common condition leading to renal dysfunction and is closely related to increased cardiovascular and mortality risk. CKD is an important public health issue, and recent genetic studies have verified common CKD susceptibility variants. This research examines the interrelationship between candidate genes polymorphisms of interferon lambda (IFNL) induction, its signaling pathway, and CKD. Methods: Seventy-five patients with advanced CKD and 312 healthy subjects (as controls) participated in this research. A replication set composed of 172 patients with advanced CKD and 365 controls was used for additional analysis. The genotype of single nucleotide polymorphisms (SNPs) was determined by the Axiom Genome-Wide Human Assay and SNaPshot assay. Results: The SNP of IFNL3 was significantly associated with CKD in the codominant (p = 0.02) and dominant models (p = 0.02). In addition, the SNPs of IFNL2 were significantly associated with CKD in the dominant model (p = 0.03), and the SNP of interferon alpha receptor 2 (IFNAR2) was significantly associated with CKD in the log-additive model (p = 0.03). Concerning rs148543092, in the IFNL3 gene, a significant association was observed after pooling the original and replication sets. Conclusion: These results indicate that SNPs in the IFNL induction and signal pathway may be associated with CKD risk in the Korean population. Finally, our results also show that the IFNL3 gene variant may be associated with CKD risk.

Background: Recurrent glomerulonephritis (GN) is a common cause of allograft loss in kidney transplantation (KT), the most frequent of which is immunoglobulin A (IgA) nephropathy (IgAN). Galactose-deficient IgA1 (Gd-IgA1) plays a major role in the pathophysiology of IgAN, but the association between Gd-IgA1 and recurrent IgAN in kidney transplant recipients (KTRs) is uncertain. We aimed to evaluate the efficacy of Gd-IgA1 for prediction of recurrent IgAN and graft and patient survival according to Gd-IgA1 level. Methods: We enrolled 27 KTRs who underwent allograft biopsy between 2009 and 2016 and measured the serum Gd-IgA1 level of each KTR. We divided the patients into two groups: nonrecurrent IgAN (patients with IgAN prior to KT who were not diagnosed with recurrent IgAN) and recurrent IgAN (patients with IgAN prior to KT who were diagnosed with recurrent IgAN). Results: The mean serum Gd-IgA1 level was significantly higher in the recurrent IgAN group than in the nonrecurrent IgAN group (6,419 ± 3,675 ng/mL vs. 3,381 ± 2,844 ng/mL, p = 0.02). The cutoff value of serum Gd-IgA1 in receiver operating characteristic curve analysis was 4,338 ng/mL (area under the curve, 0.76; 95% confidence interval [CI], 0.57–0.95, p = 0.02). Serum Gd-IgA1 level was an independent factor for recurrent IgAN (odds ratio, 17.60; 95% CI, 1.33–233.03, p = 0.03). There was no significant difference in graft or patient survival between the two groups. Conclusion Serum Gd-IgA1 can be used as a diagnostic biomarker for recurrent IgAN in KT.

Background: Recurrent glomerulonephritis (GN) is a common cause of allograft loss in kidney transplantation (KT), the most frequent of which is immunoglobulin A (IgA) nephropathy (IgAN). Galactose-deficient IgA1 (Gd-IgA1) plays a major role in the pathophysiology of IgAN, but the association between Gd-IgA1 and recurrent IgAN in kidney transplant recipients (KTRs) is uncertain. We aimed to evaluate the efficacy of Gd-IgA1 for prediction of recurrent IgAN and graft and patient survival according to Gd-IgA1 level. Methods: We enrolled 27 KTRs who underwent allograft biopsy between 2009 and 2016 and measured the serum Gd-IgA1 level of each KTR. We divided the patients into two groups: nonrecurrent IgAN (patients with IgAN prior to KT who were not diagnosed with recurrent IgAN) and recurrent IgAN (patients with IgAN prior to KT who were diagnosed with recurrent IgAN). Results: The mean serum Gd-IgA1 level was significantly higher in the recurrent IgAN group than in the nonrecurrent IgAN group (6,419 ± 3,675 ng/mL vs. 3,381 ± 2,844 ng/mL, p = 0.02). The cutoff value of serum Gd-IgA1 in receiver operating characteristic curve analysis was 4,338 ng/mL (area under the curve, 0.76; 95% confidence interval [CI], 0.57–0.95, p = 0.02). Serum Gd-IgA1 level was an independent factor for recurrent IgAN (odds ratio, 17.60; 95% CI, 1.33–233.03, p = 0.03). There was no significant difference in graft or patient survival between the two groups. Conclusion Serum Gd-IgA1 can be used as a diagnostic biomarker for recurrent IgAN in KT.

Tolvaptan, a non-peptide arginine vasopressin V2 receptor antagonist, is a newly developed drug to reduce kidney volume and preserve kidney function in autosomal dominant polycystic kidney disease (ADPKD) patients. We aimed to evaluate the descriptive characteristics of patients according to the use of tolvaptan. Also, we tried to find the efficacy of tolvaptan on kidney volume and kidney function. We included patients with ADPKD who visited a tertiary hospital in South Korea during Sep. 2018 and Apr. 2022. The data was acquired from the Electric Medical Records system. A total of 64 patients were included in the study, and there were 33 (51.6%) patients taking tolvaptan during follow-up periods. During 17.8 ± 13.1 months of follow-up periods, estimated glomerular filtration rate (eGFR) changes were 89.4% compared to the baseline eGFR. Although the latest eGFR was lower in patients with tolvaptan (55.9 ± 24.7 mL/min/1.73 m2) than without tolvaptan (68.4 ± 35.1 mL/min/1.73 m2), there was no statistical significance (p = 0.108). We found that the mean change of height-adjusted total kidney volume (HtTKV) was -2.7% based on the baseline HtTKV in patients taking tolvaptan for more than 1-year. Although there was no statistical significance, the mean change of HtTKV was the highest in patients with 1E of Mayo classification (-4.3%). To anticipate the solid data on the efficacy of tolvaptan in the Asian population, more aggressive efforts are needed to search for suitable patients accompanied by appropriate monitoring over a more extended period.

The widespread use of colonoscopy for early detection of colorectal pathology has increased the use of osmotic laxatives for colonic cleansing. Among these, oral sodium phosphate preparations can cause renal insufficiency through the development of acute phosphate nephropathy. Acute phosphate nephropathy can be distinguished as early symptomatic and late insidious patterns. Patients whose presentation is insidious are easily overlooked and can progress to chronic kidney disease. We report a case of complete recovery from the late insidious type of acute phosphate nephropathy.
Colon ; Colonoscopy ; Humans ; Laxatives ; Pathology ; Renal Insufficiency ; Renal Insufficiency, Chronic ; Sodium

BACKGROUND: Although kidney transplantation outcomes have improved dramatically after using calcineurin inhibitors (CNIs), CNI toxicity continues to be reported and the mechanism remains uncertain. Here, we investigated the neurotoxicity of CNIs by focusing on the viability of glioma cells.METHODS: Glioma cells were treated with several concentrations of CNIs for 24 hours at 37℃ and their cell viability was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.RESULTS: Exposure to 0, 0.25, 0.5, 2.5, 5.0, and 10.0 mM concentrations respectively showed 100%, 64.3%, 61.3%, 68.1%, 62.4%, and 68.6% cell viability for cyclosporine and 100%, 38.6%, 40.8%, 43.7%, 37.8%, and 43.0% for tacrolimus. The direct toxic effect of tacrolimus on glioma cell viability was stronger than that of cyclosporine at the same concentration.CONCLUSION: CNIs can cause neurological side effects by directly exerting cytotoxic effects on brain cells. Therefore, we should carefully monitor the neurologic symptoms and level of CNIs in kidney transplant patients.
Animals ; Brain ; Calcineurin Inhibitors ; Calcineurin ; Cell Survival ; Cyclosporine ; Glioma ; Humans ; Kidney ; Kidney Transplantation ; Neurologic Manifestations ; Rats ; Tacrolimus

BACKGROUND: Although kidney transplantation outcomes have improved dramatically after using calcineurin inhibitors (CNIs), CNI toxicity continues to be reported and the mechanism remains uncertain. Here, we investigated the neurotoxicity of CNIs by focusing on the viability of glioma cells. METHODS: Glioma cells were treated with several concentrations of CNIs for 24 hours at 37℃ and their cell viability was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. RESULTS: Exposure to 0, 0.25, 0.5, 2.5, 5.0, and 10.0 mM concentrations respectively showed 100%, 64.3%, 61.3%, 68.1%, 62.4%, and 68.6% cell viability for cyclosporine and 100%, 38.6%, 40.8%, 43.7%, 37.8%, and 43.0% for tacrolimus. The direct toxic effect of tacrolimus on glioma cell viability was stronger than that of cyclosporine at the same concentration. CONCLUSION CNIs can cause neurological side effects by directly exerting cytotoxic effects on brain cells. Therefore, we should carefully monitor the neurologic symptoms and level of CNIs in kidney transplant patients.

Tuberculosis (TB) of the genitourinary system is a rare form of extrapulmonary TB. Testicular TB is particularly uncommon among kidney transplantation (KT) recipients. Diagnosing testicular TB is challenging due to the nonspecific nature of clinical presentations and ambiguous imaging results. In this report, we describe a case involving a 36-year-old male KT recipient who presented with left scrotal pain. He had undergone a living donor KT 8 years prior and was receiving tacrolimus, mycophenolate mofetil, and prednisolone. Laboratory tests revealed anemia, leukocytosis, and elevated inflammatory markers. Computed tomography showed left scrotal wall thickening and enlargement, suggestive of a left testicular abscess. We discontinued mycophenolate mofetil and administered intravenous antibiotics. Additionally, we performed an incision and drainage of the abscess. However, there was no improvement in his clinical course. Consequently, we performed a radical left orchiectomy. The biopsy revealed extensive chronic granulomatous inflammation with caseous necrosis, consistent with tuberculous orchiepididymitis. A quadruple anti-TB regimen was administered, leading to an improvement in the patient's condition. To the best of our knowledge, this is the first reported case of testicular TB without other organ involvement in KT recipients. Including testicular TB in the differential diagnosis of testicular infections and masses is necessary to avoid unnecessary surgical procedures.

Tuberculosis (TB) of the genitourinary system is a rare form of extrapulmonary TB. Testicular TB is particularly uncommon among kidney transplantation (KT) recipients. Diagnosing testicular TB is challenging due to the nonspecific nature of clinical presentations and ambiguous imaging results. In this report, we describe a case involving a 36-year-old male KT recipient who presented with left scrotal pain. He had undergone a living donor KT 8 years prior and was receiving tacrolimus, mycophenolate mofetil, and prednisolone. Laboratory tests revealed anemia, leukocytosis, and elevated inflammatory markers. Computed tomography showed left scrotal wall thickening and enlargement, suggestive of a left testicular abscess. We discontinued mycophenolate mofetil and administered intravenous antibiotics. Additionally, we performed an incision and drainage of the abscess. However, there was no improvement in his clinical course. Consequently, we performed a radical left orchiectomy. The biopsy revealed extensive chronic granulomatous inflammation with caseous necrosis, consistent with tuberculous orchiepididymitis. A quadruple anti-TB regimen was administered, leading to an improvement in the patient's condition. To the best of our knowledge, this is the first reported case of testicular TB without other organ involvement in KT recipients. Including testicular TB in the differential diagnosis of testicular infections and masses is necessary to avoid unnecessary surgical procedures.

Tuberculosis (TB) of the genitourinary system is a rare form of extrapulmonary TB. Testicular TB is particularly uncommon among kidney transplantation (KT) recipients. Diagnosing testicular TB is challenging due to the nonspecific nature of clinical presentations and ambiguous imaging results. In this report, we describe a case involving a 36-year-old male KT recipient who presented with left scrotal pain. He had undergone a living donor KT 8 years prior and was receiving tacrolimus, mycophenolate mofetil, and prednisolone. Laboratory tests revealed anemia, leukocytosis, and elevated inflammatory markers. Computed tomography showed left scrotal wall thickening and enlargement, suggestive of a left testicular abscess. We discontinued mycophenolate mofetil and administered intravenous antibiotics. Additionally, we performed an incision and drainage of the abscess. However, there was no improvement in his clinical course. Consequently, we performed a radical left orchiectomy. The biopsy revealed extensive chronic granulomatous inflammation with caseous necrosis, consistent with tuberculous orchiepididymitis. A quadruple anti-TB regimen was administered, leading to an improvement in the patient's condition. To the best of our knowledge, this is the first reported case of testicular TB without other organ involvement in KT recipients. Including testicular TB in the differential diagnosis of testicular infections and masses is necessary to avoid unnecessary surgical procedures.