
Distinguishing tubulointerstitial nephritis (TIN) from acute tubular necrosis (ATN) is clinically important in Legionella-associated acute kidney injury (AKI), because TIN may respond to corticosteroid therapy whereas ATN does not. However, kidney biopsy is often not feasible in critically ill patients, and noninvasive approaches to guide treatment decisions are needed. We report a 73-year-old man with severe Legionella pneumonia complicated by dialysis-dependent AKI persisting for more than one month despite resolution of the infection and discontinuation of all antibiotics by Day 9. Markedly elevated urinary beta2-microglobulin (118,539 μg/L at Day 28) and diffuse intense bilateral renal uptake on gallium-67 scintigraphy (grade 5, clearly exceeding liver and vertebral body uptake) on Day 31 supported ongoing renal inflammation in the setting of prolonged tubular injury. A diagnostic trial of prednisolone (0.5 mg/kg/day) was initiated; from approximately 1 week later, urine output increased, serum creatinine declined, and hemodialysis was successfully discontinued on Day 43. Renal function returned to pre-illness baseline by Day 57 (serum creatinine 0.75 mg/dL). Kidney biopsy performed after clinical stabilization showed acute tubular injury with chronic tubulointerstitial changes and a focal, reactive T-cell infiltrate; prior or partially treated TIN could not be excluded. This case shows that renal recovery remains possible in Legionella-associated AKI even after more than 1 month of dialysis dependence, and suggests that gallium-67 scintigraphy, interpreted alongside serial urinary tubular injury markers, may provide ancillary evidence of ongoing renal inflammation when biopsy is not immediately feasible.
Vitamin D receptor activators (VDRAs) are widely prescribed for osteoporosis and CKD-mineral and bone disorder in Japan. Although hypercalcemia and acute kidney injury (AKI) are recognized adverse effects, metabolic alkalosis in these patients has received limited attention as a feature of calcium-alkali syndrome (CAS).We retrospectively reviewed patients with VDRA-associated hypercalcemia at our institution between April 2016 and June 2026, applying study-defined operational criteria for a CAS-like phenotype: hypercalcemia, elevated bicarbonate compatible with a metabolic alkalosis component (HCO₃⁻ ≥ 26 mmol/L), and AKI (KDIGO criteria). Seven elderly women fulfilled all criteria. Six received eldecalcitol (0.75 μg/day) and one received alfacalcidol (1.0 μg/day). Underlying CKD was present in six patients.Time from initiation to onset ranged from 1 to 120 months (median 18 months). Three cases had no identified exogenous alkali source. The serum Na–Cl difference was elevated in all patients (range 36–53 mEq/L). Renal outcomes were complete recovery in three patients, partial recovery in two, and non-recovery in one; one patient died of worsening heart failure.VDRA-associated hypercalcemia can present as a CAS-like phenotype even without calcium supplementation, and renal outcomes may be irreversible. Because the temporal relationship between hypercalcemia and metabolic alkalosis cannot be established from these retrospective data, the main clinical message is that elderly patients receiving VDRAs, particularly those with CKD or relevant concomitant medications, require periodic calcium monitoring and prompt evaluation when nonspecific symptoms, AKI, or an elevated Na–Cl difference are observed.
Renal vein thrombosis (RVT) is a rare and underrecognized complication of acute pyelonephritis, with nephrotic syndrome and malignancy remaining the predominant causes of RVT. Because its clinical features overlap with those of the underlying infection, the diagnosis is often delayed until thrombus propagation or embolization occurs. A previously healthy 29-year-old man presented with a two-week history of left flank pain and fever. Contrast-enhanced computed tomography demonstrated acute left pyelonephritis with extensive renal vein thrombosis extending into the suprarenal inferior vena cava. Despite initiation of anticoagulation, pulmonary embolism developed during hospitalization. Cultures did not identify a causative organism; a low-count Staphylococcus haemolyticus isolate was considered a contaminant. Thrombophilia screening was negative. The patient improved with antimicrobial therapy and anticoagulation alone, requiring no invasive intervention. A PubMed search identified 23 previously published cases of acute pyelonephritis-associated RVT, pooled with the present case (n = 24) and analyzed separately from five xanthogranulomatous pyelonephritis-associated cases. Three cases were excluded for systemic or multifactorial thrombosis, and one case of RVT radiologically mimicking pyelonephritis. Gram-negative organisms predominated (78.3
Kocuria kristinae is a commensal skin bacterium that occasionally acts as an opportunistic pathogen. However, it is rarely associated with pericardial infection. This report describes the case of a 47-year-old male patient with dialysis-dependent acute kidney injury (AKI) complicated by massive inflammatory pericardial effusion, in whom K. kristinae was isolated. The patient developed a severe heatstroke, which was followed by AKI, subsequently requiring hemodialysis. Approximately 1 month later, the cardiothoracic ratio increased markedly, and echocardiography revealed substantial pericardial effusion. Anti-inflammatory therapy, comprising non-steroidal anti-inflammatory drugs, colchicine, and prednisolone, elicited a poor response, given no improvement in the effusion. Ultrasound guidance was used for pericardiocentesis, resulting in drainage of 1050 mL of pale-yellow, exudative fluid with neutrophil predominance. K. kristinae was subsequently identified using the VITEK 2 system. The vancomycin dosage was determined based on the susceptibility results. Following the implementation of drainage and antimicrobial therapy, pericardial effusion decreased, venous congestion was alleviated, and urine output increased. These interventions may have contributed to renal recovery and the discontinuation of hemodialysis on day 102. Clinicians should regard K. kristinae isolated from pericardial fluid as a possible contaminant notwithstanding a clinically compatible setting. This case suggests that a massive pericardial effusion with venous congestion can delay renal recovery in severe AKI, whereas successful pericardial drainage facilitates recovery of urine output and withdrawal from hemodialysis.
Posttransplant lymphoproliferative disorders (PTLD) represent a heterogeneous group of lymphoproliferative lesions in patients who have solid organ or bone marrow transplantation. While majority of PTLD are of B-cell origin, T-cell PTLD is extremely rare. Monomorphic epitheliotropic intestinal T-cell lymphoma (MEITL) is a rare primary intestinal lymphoma which most commonly involves the small bowel. Since the symptoms at presentation are often vague, the diagnosis is frequently delayed until acute complications such as intestinal perforation or obstruction occur. Here we report a very rare case of posttransplant small bowel MEITL in a kidney transplant recipient presenting with protein-losing enteropathy (PLE) as the initial manifestation. Our patient initially presented with episodic diarrhea but early investigations failed to identify any bowel pathology. Subsequently she developed hypoalbuminemia-related fluid retention and Tc-99 m HSA scintigraphy confirmed the presence of PLE. Even though the upper gastrointestinal endoscopy, colonoscopy and abdominal computed tomography did not show any significant lesions, the patient developed sudden bowel perforation and histologic examination of the resected tissue confirmed the diagnosis of posttransplant MEITL. She developed severe sepsis postoperatively and finally passed away despite aggressive supportive treatment. Our case shows that early diagnosis and prompt treatment is critical to potentially improve the patient outcomes.