Groove pancreatitis (GP) is a rare type of chronic pancreatitis characterized by fibrotic lesions localized to the groove between the pancreatic head, duodenum, and common bile duct. We present a case of a 59-year-old male alcoholic with vomiting and renal dysfunction found to have duodenal obstruction and low-density pancreatic head lesions on computed tomography concerning for GP. The patient underwent pancreaticoduodenectomy and pathology confirmed the diagnosis postoperatively. The patient recovered well without complications or relapse at follow-up. Although rare, GP should be included in the differential for pancreatic head masses in middle-aged alcoholics and surgical resection may be necessary for symptom relief and exclusion of malignancy.

Pedunculated submucosal leiomyomas of the uterus that prolapse into the vagina are common. In extremely rare cases, large pedunculated submucosal leiomyomas may lead to bilateral obstructive uropathy, causing severe renal dysfunction and potentially being misdiagnosed as intracervical leiomyoma. The present study describes the surgical treatment of a patient with a large prolapsed pedunculated submucosal uterine leiomyoma, which was misdiagnosed as an intracervical fibroid. The patient, of menopausal age, presented with uterine bleeding, anemia and severe renal dysfunction. Upon a physical examination, suspicion arose for a cervical leiomyoma, prompting the decision for imaging. Both transvaginal ultrasound and computed tomography, as well as magnetic resonance imaging confirmed the diagnosis of intracervical leiomyoma, accompanied by bilateral obstructive uropathy due to ureteral compression. The surgical management of the patient with laparotomy was decided. Intraoperatively, a large pedunculated submucosal uterine leiomyoma prolapsing into the vagina was identified. Total hysterectomy and bilateral salpingectomy-oophorectomy were performed. The immediate post-operative course was uneventful. At 6 months following surgery, the complete recovery of renal morphology and function was observed. The patient continues to undergo regular follow-up assessment to date. In the present study, a brief literature review is also provided, emphasizing the significant diagnostic and surgical challenges that may arise in the management of patients with large pedunculated submucosal uterine leiomyomas prolapsing into the vagina.

Autoimmune diseases may act as a trigger for atypical hemolytic uremic syndrome (aHUS). Triggers for aHUS may include autoimmune diseases, infections, metabolic conditions, pregnancy, and transplants. aHUS-mediated injury to various organs, especially kidneys, can be life-threatening. Here, we present the case of a young female who had perinuclear antineutrophil cytoplasmic antibody (p-ANCA)-associated vasculitis and was diagnosed with aHUS. We consider underlying autoimmune p-ANCA-associated vasculitis as a trigger for aHUS in this case.

The non-ketotic hyperglycemic chorea (NKHC) was a rare complication for patients with diabetes mellitus, but not been well studied. In the present research, we aimed to investigate the clinical and imaging characteristics of NKHC and explore the potential association.
We performed a case-control study with patients diagnosed as NKHC. The patients with group of NKHC were retrospectively recruited, while the matched group were set to screened patients with diabetes mellitus but no NKHC at a 1:3 ratio. The clinical and imaging data were collected for all the participants of the two groups. Firstly, Correlation analysis was conducted to test the difference of all the variables between the NKHC group and matched group. Then, the putative associated factors for NKHC were further identified.
Eleven men and 9 women with NKHC and 60 matched participants were analyzed. The mean age of the NKHC group was 68.5 ± 14.9 years. Participants with NKHC were more likely to have a higher glycosylated hemoglobin (HbA1c) level (13 ± 2.82 vs. 10.57 ± 2.71, P<0.001), and a higher frequency of renal dysfunction (estimated glomerular filtration rates <60 ml/min/1.73m2) (55% vs. 20%, P=0.005). Logistic regression analyses showed that both higher HbA1c and renal dysfunction were significantly correlated with NKHC.
A higher value of HbA1c and renal dysfunction may be associated with the occurrence of NKHC.

A 70-year-old female patient was admitted for close examination and treatment of hypercalcemia (corrected serum calcium levels: 3.04 mmol/L) and renal dysfunction (serum creatinine levels: 254.59 µmol/L). The patient had a history of sarcoidosis, diagnosed based on epithelioid cell granulomas in subcutaneous nodule biopsies, uveitis, and bilateral hilar lymphadenopathy, which had spontaneously remitted 10 years before admission. Because the patient was diagnosed with hypercalcemia associated with recurrent sarcoidosis, prednisone (20 mg/day) was initiated, and its dose was tapered following the decrease in serum calcium and creatinine levels. However, the levels of these parameters increased again when the prednisone dose was reduced to ≤ 4 mg/day. We were concerned about glucocorticoid-induced osteoporosis in the patient but hesitated to use first-line bisphosphonates because of renal dysfunction. Therefore, denosumab was initiated to reduce the risk of hypercalcemia, renal dysfunction, and glucocorticoid-induced osteoporosis. Serum creatinine and corrected serum calcium levels subsequently decreased. The prednisone dose could be reduced following repeated denosumab administration.Thus, denosumab can be a multifaceted, beneficial option for sarcoidosis-induced hypercalcemia, as it alleviates renal dysfunction indirectly by normalizing serum calcium levels, facilitates reduction of the glucocorticoid dose, and ameliorates glucocorticoid-induced osteoporosis.

An 80-year-old man presented with electrolyte abnormalities, particularly hypocalcemia (3.6 mg/dL). He was diagnosed with bone and lymph node metastases from prostate cancer seven years earlier and continuously received goserelin, bicalutamide, and zoledronate. He later developed gradually worsening hypocalcemia, hypokalemia, hypophosphatemia, hypouricemia, renal dysfunction, and weight loss. Urinary potassium and phosphate loss, renal glucosuria, metabolic acidosis, and a low urine pH (5.0) were observed. Given the acquired onset and clinical course, we diagnosed the patient with zoledronate-induced proximal renal tubular acidosis. In the present case, severe hypocalcemia may have been caused by malnutrition and inappropriate long-term use of zoledronate.

We report a case of a 34-year-old male with severe multisystemic involvement (including the testis, musculoskeletal system, skin, upper respiratory tract, ocular system, peripheral nerves, abdomen, and kidney) due to granulomatosis with polyangiitis (GPA) and a high proteinase 3 (PR3)-antineutrophil cytoplasmic antibodies (PR3ANCA) titer. A renal biopsy showed pauci-immune glomerulonephritis (GN). Systemic corticotherapy combined with cyclophosphamide was chosen for induction therapy. During the induction phase, clinical deterioration occurred in the form of severe alveolar hemorrhage, leading to admission to the intensive care unit (ICU). Influenza A (H1N1) was detected in the respiratory tract. Furthermore, blood sampling revealed an invasive Klebsiella pneumoniae infection that persisted despite multiple antibiotic regimens. A CT scan showed splenic vascular compromise, assumed to be the primary source of the infection, with sustained improvement after splenectomy. Maintenance therapy included a tapering dose of corticotherapy for 36 months and azathioprine 100mg daily for five years, which achieved full and sustained remission. The patient has been in full remission for nine years, with mild renal sequelae, including proteinuria and secondary hypertension.

Collagenofibrotic glomerulopathy (CG) is a poorly understood kidney disease characterized by extensive deposition of abnormal type III collagen within the glomeruli. We report the case of a 25-year-old man with known type I diabetes mellitus who presented to the emergency department with diaphoresis, nephrotic-range proteinuria, hypertension, and elevated creatinine. Renal biopsy revealed combined collagenofibrotic glomerulopathy and diabetic nephropathy. This case highlights the clinicopathological features of type III collagen glomerulopathy and its possible association with diabetic nephropathy.

Milk-alkali syndrome, which is characterized by hypercalcemia, metabolic alkalosis, and renal dysfunction, typically results from the ingestion of large amounts of calcium and absorbable alkaline products. However, these symptoms can also manifest when alkalosis and calcium loading occur simultaneously, owing to other factors. We report a case of milk-alkali syndrome caused by loop-diuretic-induced alkaline load and polypharmacy in an 85-year-old Japanese woman with multiple comorbidities, including osteoporosis, hypertension, type 2 diabetes, dyslipidemia, and Parkinson\'s disease. The patient regularly took 14 drugs, including calcium L-aspartate, eldecalcitol, celecoxib, and a fixed-dose combination of losartan and hydrochlorothiazide. Immediately before admission, furosemide was administered for the treatment of edema. The patient presented with chest discomfort, general malaise, and clinical signs of dehydration, hypercalcemia, hypophosphatemia, hypokalemia, and hypomagnesemia, accompanied by electrocardiogram abnormalities, renal dysfunction, and chloride-resistant metabolic alkalosis. The hypercalcemia was specifically induced by calcium L-aspartate and eldecalcitol. The hypomagnesaemia and hypophosphatemia were caused by diuretics and hypercalcemia. Thus, all the oral medications were discontinued, and rehydration and electrolyte correction therapy were administered. The final diagnosis was milk-alkali syndrome caused by the concomitant use of loop diuretics and other medications, without absorbable alkaline preparation use. This case underscores the importance of considering drug-related factors, checking concomitant medications, and being aware of the benefits, harmful effects, and side effects of polypharmacy in older adults with multimorbidity.

Pelvic organ prolapse is rarely associated with severe bilateral ureteral hydronephrosis and renal dysfunction. The etiopathogenetic mechanism has not been fully elucidated. Contemporary imaging methods of the urinary tract play a decisive role in assessing the morphological function of the kidneys. In cases of moderate and severe pelvic organ prolapse, surgery appears to be the main choice of treatment. Our case concerns a post-menopausal patient with three vaginal deliveries in her obstetric history and with a history of bilateral hydronephrosis and impaired renal function who was referred to the outpatient clinic for a gynecological examination due to complete uterine prolapse. Bilateral hydroureteronephrosis due to prolapse was assessed as the main cause of renal dysfunction. A surgical intervention was decided to the pelvic floor and a vaginal hysterectomy was performed with simultaneous correction of the cystocele and rectocele. The postoperative course was uneventful. Three months later, re-examination of the urinary tract showed complete remediation of kidney morphology and function. The present case report emphasizes the significant degree of bilateral hydroureteronephrosis and deterioration of renal function rarely seen in patients with complete uterine prolapse. At the same time, it is pointed out that the exclusion of renal dysfunction related to complete uterine prolapse should be the main concern of the modern gynecologist even for complex cases with coexisting etiological factors for renal disease, in order to avoid permanent renal parenchymal damage and ensure the best health and quality of life of these patients.