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Glucose and electrolytes levels were within normal values, as were urea and creatinine levels, suggesting kidney function was unchanged.
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Because high levels of urine sCD163 often suggest kidney injury and a bad prognosis, urine sCD163 could be employed to assess the prognosis in patients who develop AKI.
Elevated serum levels of blood urea nitrogen (BUN), creatinine and phosphorous (Fig. 2A) suggested kidney dysfunction, although upon histological analysis no obvious lesions in the kidneys were noted (not shown).
Only 119 people (0.2%) had creatinine > 2.50 mg/dL, which suggests kidney disease that can affect uric acid; excluding these participants from the analyses did not change the results.
Surprisingly, our patient presented with severe PH several years after successful kidney transplantation, suggesting that kidney transplantation per se does not necessarily prevent the abnormal haemodynamics associated with A-V access fistulas.
Furthermore, the systematic downregulation of Msi1/Msi2 and high frequency of Msi1 mutations in kidney tumors suggests that kidney would be an informative model for studying Msi loss-of-function and its consequences in cancer.
Finally, 42.1% of AKI survivors had albuminuria during follow-up in the POST-RENAL study suggesting persisting kidney damage in these patients [183].
Clinical symptoms suggesting acute kidney injury (AKI) occur late, but the pathology may quickly progress to acute renal failure.
Manipulations of LRRK2 in mouse have not generated robust neuronal phenotypes (13), with the most marked responses suggesting abnormal kidney function (14).
By 12 weeks of age, renal damage is severe, suggesting that kidney damage is accelerated in POKO mice owing to glucolipotoxicity.
Survival in silica-exposed NZM mice was decreased, with increased proteinurea levels and immunoglobulin (Ig) G deposition suggesting exacerbated kidney damage.
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