Hereditary renal hypouricemia is characterized by hypouricemia with hyper-uric acid clearance due to a defect in renal tubular transport. Patients with hereditary renal hypouricemia have a higher risk of exercise-induced acute kidney injury (EAKI) and reduced kidney function. Although the best preventive measure is avoiding exercise, there are many kinds of jobs that require occupational exercise. A 27-year-old male police officer suffered from stage 3 AKI after performing a 20-m multistage shuttle run test. His mother had previously been diagnosed as having renal hypouricemia at another facility. The patient had reported having hypouricemia during a health check at a previous police station, but his serum uric acid concentration was within the normal range at our hospital. After treatment, he recovered from EAKI and exhibited low serum uric acid and hyper-uric acid clearance. Since the patient desired to continue his career requiring strenuous exercise, it was difficult to establish a preventive plan against the recurrence of EAKI. Patients with hereditary renal hypouricemia who must undergo strenuous occupational anaerobic exercise are at higher risk of developing EAKI than other workers. The risks of EAKI among patients with hypouricemia should be considered when undergoing physical occupational training.

/pdf/exercise-induced-acute-kidney-injury-in-a-police-officer-52y6e170vl.pdf

Exercise-Induced Acute Kidney Injury in a Police Officer with Hereditary Renal Hypouricemia.

Increasingly popular, ultra-endurance participation exposes athletes to extremely high levels of functional and structural damage. Ultra-endurance athletes commonly develop acute kidney injury (AKI) and other pathologies harmful to kidney health. There is strong evidence that non-steroidal anti-inflammatory drugs, common amongst ultra-athletes, is linked to increased risk and severity of AKI and potentially ischaemic renal injury, i.e., acute tubular necrosis. Ultra-endurance participation also increases the risk of exertional rhabdomyolysis, exercise-associated hyponatremia, and gastrointestinal symptoms, interlinked pathologies all with potential to increase the risk of AKI. Hydration and fuelling both also play a role with the development of multiple pathologies and ultimately AKI, highlighting the need for individualised nutritional and hydration plans to promote athlete health. Faster athletes, supplementing nitrates, and being female also increase the risk of developing AKI in this setting. Serum creatinine criteria do not provide the best indicator for AKI for ultra-athletes therefore further investigations are needed to assess the practicality and accuracy of new renal biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL). The potential of recurring episodes of AKI provide need for further research to assess the longitudinal renal health impact of ultra-participation to provide appropriate advice to athletes, coaches, medical staff, and event organisers.

/pdf/ultra-endurance-participation-and-acute-kidney-injury-a-2sb5uy3z.pdf

Ultra-Endurance Participation and Acute Kidney Injury: A Narrative Review

In daily practice, the frequent appearance of limb and/or skin necrosis, which we term "acute peripheral and/or cutaneous ischemic syndrome" (APCIS), can be a manifestation of numerous underlying diseases, or it can sometimes be a clinical phenomenon whose etiology is undefined even after a wide investigation. The mechanisms for the development of APCIS include vessel wall abnormalities (atherosclerosis, vasculitis, and calciphylaxis), embolic processes (infectious endocarditis, atrial myxoma, and cholesterol emboli), local thrombotic injuries (genetic or acquired thrombophilias and heparin- and warfarin-induced ischemia), dysproteinemias (cryoglobulinemia and cryofibrinogenemia), or venous limb gangrene. Here, we report 5 illustrative cases of APCIS with different pathogenetic mechanisms, thereby highlighting some clinical conditions that cause APCIS that may be of special interest for rheumatologists, such as antiphospholipid syndrome, primary and secondary vasculitis, and cryoproteinemias. Furthermore, we describe a large spectrum of other causes of APCIS beyond the scope of rheumatology. Because there are no validated guidelines for APCIS, we tentatively propose an initial diagnostic workup and a therapeutic approach based on full-dose anticoagulation and immunosuppressive therapy.

Acute Peripheral and/or Cutaneous Ischemic Syndrome: What Rheumatologists Should Know.

Acute renal failure with severe loin pain and patchy renal ischemia after anaerobic exercise (ALPE) is gradually gaining recognition. In this case series, we describe the presentation of ALPE in the emergency department setting and its clinical course. In Case 1, an 18-year-old man presented with acute-onset nausea, vomiting, and right flank pain after playing basketball, with a creatinine level of 6.42 mg/dL on initial presentation. He received fluid therapy and intravenous furosemide for 2 days. His creatinine level was 1.80 mg/dL on day 8 and finally declined to 0.71 mg/dL on day 39. In Case 2, a 31-year-old man presented with acute-onset nausea and right lower abdominal pain after swimming, with a creatinine level of 4.68 mg/dL on initial presentation. He only received fluid therapy, and his creatinine level finally declined to 0.90 mg/dL on day 11. In both cases, severe loin pain began after anaerobic exercise, and acute kidney injury without myoglobinuria was observed. The findings of our case series suggest that emergency physicians should consider ALPE in the differential diagnosis of abdominal and loin pain accompanied by an elevated creatinine level in young patients because it can be treated conservatively and has a good prognosis. Moreover, watchful waiting is recommended for ALPE while also emphasizing the need to exclude potentially life threatening or treatable kidney diseases.

Acute renal failure with severe loin pain and patchy renal ischemia after anaerobic exercise

An aberrant growth of plasma cells in the bone marrow characterizes the hematological neoplasm known as multiple myeloma, which is typically accompanied by increased bone pain and skeletal-related events such as pathological fractures and/or spinal cord compression. Changes in the bone marrow microenvironment brought on by increased osteoclastic activity and/or decreased osteoblastic activity as a result of myeloma bone disease have a detrimental effect on quality of life. Bone-modifying medications such as bisphosphonates or denosumab are used to treat myeloma bone disease. These substances can lessen bone pain and the chance of pathological fracture, but they do not stimulate the growth of new bone or heal already damaged bone. In order to conduct this study, we searched the PubMed, Google Scholar, and Cochrane databases for complete free papers published in English and studied people over the previous five years, starting in 2018. The search covered randomized clinical trials (RCT), observational studies, meta-analyses, systemic reviews, and conventional reviews. Twenty-five publications are picked after using quality evaluation techniques to determine the type of study. These papers' full-text articles are investigated, examined, and tallied. We spoke about the various treatments for bone damage in multiple myeloma. It was discovered that bisphosphonates lessen the frequency and severity of bone problems. However, we are unsure of their contribution to survival. Although these medicines enhance life quality, it is unknown if they also increase overall survival. The focus of this study is on several kinds of bone-modifying drugs, their processes of action, the point at which therapy is started, how long it lasts, and any possible mortality advantages.

Multiple Myeloma and the Role of Bisphosphonates in Its Management

Acute renal failure with severe loin pain and patchy renal ischemia after anaerobic exercise (ALPE) is exercise-induced acute renal failure that occurs without myoglobinuria. We describe a typical case involving an 18-year-old man. Generally, patients with ALPE are advised to avoid anaerobic exercise due to risk of recurrence, but our patient continued and went on to become a professional cyclist without relapse. About 51% of ALPE cases involve patients with renal hypouricemia. His serum uric acid levels were rather high, at 6.4 mg/dL. He is the first patient with ALPE to succeed as a professional athlete in an anaerobic sport.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1002/jgf2.108

Exercise-induced acute renal failure in a trainee cyclist without hypouricemia: Successful athletic career post-treatment.

Optimal ferritin level in hemodialysis patients between Japan and other countries is controversial. Long-term side effects of iron supplementation in these patients remain unclear. We aimed to elucidate whether past hyperferritinemia in hemodialysis patients was associated with high risk of death and cerebrovascular and cardiovascular diseases (CCVDs). This small retrospective cohort study included approximately 44 patients unintentionally supplemented with excessive intravenous iron. A significantly higher risk of CCVDs was observed in patients with initial serum ferritin levels ≥1000 ng/mL than in the remaining patients. High ferritin levels slowly decreased to <300 ng/mL in a median of 24.2 (10.5-46.5) months without treatment. However, compared with the remaining patients, only patients whose ferritin levels did not decrease to <300 ng/mL steadily had a significantly higher risk of all-cause death (hazard ratio, 9.6). Long-term hyperferritinemia due to intravenous iron therapy is a risk factor for death in maintenance hemodialysis patients. For a prolonged better prognosis, intravenous iron should be carefully administered so as to avoid hyperferritinemia in patients with hemodialysis.

/pdf/long-term-prognosis-of-hyperferritinemia-induced-by-1lgtx9rd11.pdf

Long-Term Prognosis of Hyperferritinemia Induced by Intravenous Iron Therapy in Patients Undergoing Maintenance Hemodialysis: A 10-Year, Single-Center Study.

Although bisphosphonates are well known to cause kidney disease, there are very few published cases of focal segmental glomerulosclerosis (FSGS) following treatment with minodronate. Here we report the case of an 86-year-old woman who developed acute kidney injury and nephrotic syndrome after receiving monthly oral minodronate for 24 months. Kidney biopsy revealed cellular variant FSGS. Treatment was initiated with the discontinuation of minodronate followed by intravenous methylprednisolone pulse and prednisolone at 35 mg/day. Subsequently, the patient’s renal function gradually worsened, requiring initiation of hemodialysis. However, renal function and proteinuria improved markedly and hemodialysis was withdrawn 1 month after the initiation of steroid therapy. This is, to our knowledge, the first published case of FSGS induced by long-term use of minodronate, and also the first case of cellular variant FSGS induced by bisphosphonates although collapsing variant of FSGS is commonly caused by bisphosphonates. Our study indicates that patients on bisphosphonates should be closely monitored for proteinuria and renal impairment, regardless of the type of bisphosphonate.

Nephrotic syndrome with acute kidney injury due to focal segmental glomerulosclerosis following long-term treatment with minodronate.

A 57-year-old female was admitted with renal insufficiency (serum creatinine level, 11.1 mg/dL) accompanied with nephrotic syndrome (total protein/creatinine ratio in spot urine specimen, 6.23 g/gCr), hematuria, and nonpalpable purpura (Fig. 1a). The first biopsy of the lesions on her upper legs did not show evidence of vasculitis, likely due to the inappropriate choice of the biopsy site. The necrotic skin lesions progressed daily, resembling purpura fulminans, which typically occur in acute infections [1]. However, unlike typical purpura fulminans, the patient’s symptoms were not accompanied by disseminated intravascular coagulation or circulatory collapse. Bacterial infection, medications, autoantibodies, thrombocytopenia, and coagulation abnormalities were ruled out as the etiology. The second skin biopsy of the purpuric lesions on her back revealed leukocytoclastic vasculitis (Fig. 1b). Immunoglobulin A (IgA) deposition was not observed, possibly due to the presence of necrosis in the lesions; however, based on the renal insufficiency and high IgA level, she was diagnosed with IgA vasculitis. After the steroid therapy initiation, the necrosis progression halted and the purpuric lesions disappeared immediately, although her renal function did not improve. IgA vasculitis usually accompanies palpable purpura [2]. The presentation of the current case resembled purpura fulminans which usually accompanies nonpalpable purpura [1, 3], and vasculitis was not suspected; however, the exclusion of other causes of purpura led to the definitive diagnosis. Repeated skin biopsies are necessary for patients with suspicious vasculitis or purpura fulminans.

Vasculitis with nonpalpable purpura resembling purpura fulminans.

An 81-year-old female patient underwent an emergent surgery because of small intestinal perforation Within a 5-mm-sized hole in ileum, a half-folded, empty polyethylene drug-wrapping film with the drug names, date, and her name was found

Small intestinal perforation caused by folded polyethylene drug-wrapping film.

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