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Zinner syndrome (ZS) is a rare congenital urological condition characterized by a triad of ipsilateral seminal vesicle cysts, unilateral renal agenesis, and ejaculatory duct obstruction, first described in 1914. This case report details the presentation and management of a 27-year-old male diagnosed with ZS following a 2-month history of urinary frequency, hesitancy, dysuria, and painful ejaculation. Physical examination revealed a left lower abdominal mass, and imaging confirmed the classic findings of ZS, including unilateral renal agenesis, an enlarged seminal vesicle cyst, and an ectopic ureter.

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Pseudohypoaldosteronism (PHA) is a rare disorder that mimics congenital adrenal hyperplasia (CAH). Renal type A1A of the disorder has a known gene mutation (NR3C2) and parents may be asymptomatic despite biochemical abnormalities. Meticulous interpretation of hormonal and biochemical data, and early liaison with endocrinology and renal teams are key in diagnosis.

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Zinner syndrome is a congenital anomaly characterized by seminal vesicle cysts, ipsilateral renal agenesis, and ejaculatory duct obstruction possibly associated with infertility. Only 200 cases of Zinner syndrome have been reported since its discovery in 1914. We present the case of a 63-year-old man seeking treatment for a ureteropelvic junction stone causing severe hydronephrosis.

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Chronic kidney disease (CKD) is a prevalent global health concern affecting approximately 850 million people worldwide, with a significant and rising mortality rate. CKD often coexists with hyperuricemia (HSUA), which is also increasingly common due to its association with hypertension, obesity, and diabetes. The interplay between hyperuricemia and CKD is complex; while in vitro studies and animal models support a role for uric acid mediating glomerular and tubule-interstitial damage, and HSUA has been shown to predict the onset and progression of CKD, the expectations of renal protection by the use of urate lowering treatment (ULT) are inconsistent.

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