Serial changes in splenic volume of 25 patients (18 men and seven women; 53.4 +/- 20.8 years old, range 25-83) with acute pancreatitis who underwent CT examinations were retrospectively studied. Abdominal CT was performed within 3 days after the onset and there was at least one follow-up CT examination after this time. The percentage changes of splenic volume in the first (4-30 days) and second (31-100 days) follow-up CT were calculated. Splenic volume increased in the first follow-up CT (mean +/- SD: 197.8 +/- 121.0 cm3) compared with the initial CT (124.8 +/- 70.0; p < 0.0001), and then decreased in the second follow-up CT (179.7 +/- 100.7; p < 0.002). The average splenic volume increased 65.5 +/- 88.7% (range -10.4-377.4%) between the initial and first follow-up CT examinations. Five of 25 cases (20%) in whom size of spleen increased more than twice had severe acute pancreatitis (p < 0.05), complicated pseudocyst requiring surgical drainage (p < 0.05), pleural effusion (p < 0.01), splenic vein thrombosis or compression (p < 0.05) and longer hospital stay (p < 0.02) compared with patients with a smaller increase in splenic volume. In conclusion, transient splenomegaly was commonly seen in acute pancreatitis, especially in severe or complicated cases. Congestive splenomegaly caused by obstruction or stenosis of the splenic vein and non-specified acute splenitis were suspected of contributing to the transient splenomegaly.

Recent randomized trials demonstrating the beneficial effects of sodium-glucose cotransporter 2 inhibitors (SGLT2is) in type 2 diabetes suggest that early reductions in eGFR upon initiation of SGLT2i therapy are associated with improved renal outcomes. Multiple concomitant medications, including antidiabetic and antihypertensive agents, are commonly used, however, which may modify the renal hemodynamic action of SGLT2is. Here we found that background treatment with metformin diminished the SGLT2i-induced reductions in eGFR after 3 months of SGLT2i therapy in patients with type 2 diabetes and hypertension (−2.29 ± 0.90 vs −5.85 ± 1.27 mL/min/1.73 m2 for metformin users (n = 126) and nonusers (n = 97), respectively). Other antidiabetic agents (DPP4 inhibitors, sulfonylureas and insulin) had no effect on the eGFR response to SGLT2is. Antihypertensive drugs, including calcium channel blockers (CCBs) and β blockers, did not affect the SGLT2i-induced changes in eGFR, whereas renin-angiotensin system inhibitors (RASis) tended to enhance this response (p = 0.059). Next, we evaluated the interaction between metformin and RASis in the eGFR responses to SGLT2is. Under no background treatment with RASis, metformin abrogated the eGFR response to SGLT2is, but this response was preserved when RASis had been given along with metformin (decreases of 0.75 ± 1.28 vs. 4.60 ± 1.15 mL/min/1.73 m2 in eGFR, p = 0.028). No interaction between metformin and insulin or between metformin and DPP4 inhibitors was observed. In conclusion, metformin blunts the SGLT2i-induced decrease in eGFR, but coadministration of RASis ameliorates this response. Furthermore, the inability of CCBs to modify the SGLT2i-induced reduction in eGFR suggests that the SGLT2i-induced renal microvascular action is mediated predominantly by postglomerular vasodilation rather than preglomerular vasoconstriction.

Keywords： amantadine, hypoalbuminemia, blood purification, acute kidney injury, malignant syndrome 〈Abstract〉 Amantadine is widely used to treat Parkinson's disease. However, it should not be used in patients with impaired renal function since it is almost exclusively metabolized through renal excretion. We experienced a rare case of amantadine intoxication in a patient with Parkinson's disease and nephrotic syndrome. A 71-year-old patient initially had normal renal function(eGFR： 62 mL/min/1.73 m 2)and received the optimal dose of amantadine(150 mg/day). The patient then developed new-onset nephrotic syndrome with severe hypoalbuminemia(1.6 g/dL) , which was complicated by an acute kidney injury. This resulted in amantadine intoxication. Treatment with both direct hemoperfusion(DHP)and hemodiafiltration(HDF)effectively reduced the patient's serum amantadine concentration； however, this caused neuroleptic malignant syndrome, which manifested as disturbed con

Background We report a case of acute renal failure with loin pain and patchy renal ischemia after anaerobic exercise (ALPE) caused by sudden training resumption. Case presentation A 19‐year‐old Asian man who was a college American football player presented with severe back pain, headache, and malaise. He developed acute kidney injury without myoglobinuria. Based on the typical medical history and symptoms, we made a diagnosis of ALPE. Symptoms improved within a few days, and serum creatinine levels improved after discharge. He resumed training, adjusting his load step by step. Conclusion During the coronavirus disease 2019 pandemic, many athletes were unable to undergo adequate training. Long‐term de‐training leads to decreased various organ function and reduces the anaerobic threshold. Rapid resumption after prolonged de‐training may put individuals at risk of developing ALPE.

Background Hypertensive emergency is a critical disease that causes multifaceted sequelae, including end-stage kidney disease and cardiovascular disease. Although the renin–angiotensin–aldosterone (RAA) system is enormously activated in this disease, there are few reports that attempt to characterize the effect of early use of RAA inhibitors (RASi) on the temporal course of kidney function. Methods This retrospective cohort study was conducted to clarify whether the early use of RASi during hospitalization offered more favorable benefits on short-term renal function and long-term renal outcomes in patients with hypertensive emergencies. We enrolled a total of 49 patients who visited our medical center with acute severe hypertension and multiple organ dysfunction between April 2012 and August 2020. Upon admission, the patients were treated with intravenous followed by oral antihypertensive drugs, including RASi and Ca channel blockers (CCB). Kidney function as well as other laboratory and clinical parameters were compared between RASi-treated and CCB- treated group over 2 years. Results Antihypertensive treatment effectively reduced blood pressure from 222 ± 28/142 ± 21 to 141 ± 18/87 ± 14 mmHg at 2 weeks and eGFR was gradually restored from 33.2 ± 23.3 to 40.4 ± 22.5 mL/min/1.73m2 at 1 year. The renal effect of antihypertensive drugs was particularly conspicuous when RASi was started in combination with other conventional antihypertensive drugs at the early period of hospitalization (2nd day [IQR: 1–5.5]) and even in patients with moderately to severely diminished eGFR (< 30 mL/min/1.73 m2) on admission. In contrast, CCB modestly restored eGFR during the observation period. Furthermore, renal survival probabilities were progressively deteriorated in patients who had manifested reduced eGFR (< 15 mL/min/1.73 m2) or massive proteinuria (urine protein/creatinine ≥ 3.5 g/gCr) on admission. Early use of RASi was associated with a favorable 2-year renal survival probability (0.90 [95%CI: 0.77–1.0] vs. 0.63 [95%CI: 0.34–0.92] for RASi ( +) and RASi (-), respectively, p = 0.036) whereas no apparent difference in renal survival was noted for CCB. Conclusions Early use of RASi contributes to the renal functional recovery from acute reduction in eGFR among patients with hypertensive emergencies. Furthermore, RASi offers more favorable effect on 2-year renal survival, compared with CCB.

Patient: Male, 59-year-old Final Diagnosis: Portal and mesenteric vein thrombosis Symptoms: Epigastric pain Medication: — Clinical Procedure: — Specialty: Gastroenterology and Hepatology Objective: Unknown ethiology Background: Non-malignant and non-cirrhotic portal and mesenteric vein thrombosis is rare. It has been reported that the hyperthyroid state is associated with increased risks of venous thrombosis due to increases in levels of various coagulation and anti-fibrinolytic factors. Particularly, changes in levels of these factors are also reported in cases of portal and mesenteric vein thrombosis. Although hyperthyroidism is not known as a risk factor for portal and mesenteric vein thrombosis, it might be an underlying pathogenesis of hyperthyroidism-associated portal and mesenteric vein thrombosis. Case Report: A 59-year-old Japanese man with a history of Grave’s disease presented with acute portal and mesenteric vein thrombosis and hyperthyroidism. Anticoagulation therapy was initiated and the dose of antithyroid drug was increased. He underwent various tests to identify causes of portal and mesenteric vein thrombosis. However, all test results were within normal range except for hyperthyroidism. Therefore, we discontinued anticoagulation therapy after normalization of thyroid hormone status. After 3 years, he experienced recurrence of portal vein thrombosis concomitant with hyperthyroidism. Conclusions: Hyperthyroidism might be associated with portal vein thrombosis. Thyroid function tests should be performed in cases of portal and mesenteric vein thrombosis in the absence of other risk factors.

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Background Hypertensive emergency is a critical disease that causes multifaceted sequelae, including end-stage kidney disease and cardiovascular disease. Although the renin-angiotensin-aldosterone (RAA) system is enormously activated in this disease, there are few reports that attempt to characterize the effect of early use of RAA inhibitors (RASi) on the temporal course of kidney function. Methods This retrospective cohort study was conducted to clarify whether the early use of RASi during hospitalization offered more favorable benefits on short-term renal function and long-term renal prognosis in patients with hypertensive emergencies. We enrolled a total of 49 patients who visited our medical center with acute severe hypertension and multiple organ dysfunction between April 2012 and August 2020. Upon admission, the patients were treated with intravenous followed by oral antihypertensive drugs, including RASi and Ca channel blockers (CCB). Kidney function as well as other laboratory and clinical parameters were compared between RASi-treated and other antihypertensive drugs-treated group over 2 years. Results Antihypertensive treatment effectively reduced blood pressure from 222 ± 4/142 ± 3 to 140 ± 3/87 ± 2 mmHg at 2 weeks and eGFR was gradually restored from 33.2 ± 3.3 to 41.1 ± 4.1mL/min/1.73m2 at 1 year. The renal effect of antihypertensive drugs was particularly conspicuous when RASi was started in combination with other conventional antihypertensive drugs at the early period of hospitalization (2nd day [IQR: 1-5.5]) and even in patients with moderately to severely diminished eGFR (< 30 mL/min/1.73 m2) on admission. In contrast, CCB modestly restored eGFR during the observation period. Furthermore, renal survival probabilities were progressively deteriorated in patients who had manifested reduced eGFR (< 15mL/min/1.73 m2) or massive proteinuria (urine protein/creatinine ≥ 3.5 g/gCr) on admission. Early use of RASi was associated with a favorable 2-year renal survival probability (0.90 [95%CI: 0.77-1.0] vs. 0.63 [95%CI: 0.34–0.92] for RASi(+) and RASi(-), respectively, p = 0.036) whereas no apparent difference in renal survival was noted for CCB, β-blocker, α-blockers, or diuretics. Conclusions Early use of RASi contributes to the renal functional recovery from acute reduction in eGFR among patients with hypertensive emergencies. Furthermore, RASi offers more favorable effect on 2-year renal survival, compared with other antihypertensive drugs.