bubble_chart Overview

Specific kidney diseases include acute tubular necrosis and acute cortical necrosis. The latter is caused by intravascular coagulation within the kidney and may lead to anuria, with a poorer prognosis. During World War II, Lücke first described a group of patients who developed acute tubular necrosis after crush injuries and shock. He believed that changes in the more distal tubules—lower nephron nephrosis—were caused by ischemia. With the application of dialysis therapy, most patients can recover (if intrarenal coagulation and cortical necrosis do not occur, patients may sometimes fully recover). Elderly patients are more prone to anuric acute renal failure in hypotensive states. Certain drugs (such as prostaglandin inhibitors—nonsteroidal anti-inflammatory drugs) appear to increase the risk of acute tubular necrosis. In some diabetic or multiple myeloma patients, mercury (especially mercuric chloride) poisoning or the use of contrast agents may lead to nonspecific acute renal failure manifestations, even if they do not develop typical lower nephron nephrosis.

bubble_chart Clinical Manifestations

The clinical manifestations are related to the clinical condition. Patients may experience hypotension and shock, but unlike prerenal renal failure, oliguria and renal failure do not improve after intravenous fluid administration. On the other hand, contrast-induced acute renal insufficiency may present with signs of excessive fluid retention. Compared to patients with chronic renal failure, those with acute renal failure less frequently exhibit symptoms of uremia (such as mental abnormalities and gastrointestinal symptoms).

bubble_chart Auxiliary Examination

① Urine: Although the specific gravity of urine is higher immediately after an acute event, it often decreases or stabilizes between 1.005 and 1.015 subsequently. The urine osmolality also decreases (<450mosm/kg，尿滲透壓/血滲透壓<1.5：1）。尿中可檢出腎小管細胞和顆粒狀管型、尿液混濁呈棕色。如果潛血試驗陽性，須注意尿中是否存在肌紅蛋白或血紅蛋白。

② Central venous pressure: Normal or grade I elevated.

③ Fluid challenge test: Urine output does not increase after intravenous infusion of mannitol or normal saline. Occasionally, low urine output may transition to high and fixed urine output (from oliguric renal failure to non-oliguric renal failure) after the use of furosemide or "renal dose" dopamine (1–5 μg/kg/min), but the elevated blood urea nitrogen or creatinine ratio usually remains unchanged.

bubble_chart Treatment Measures

If the initial stage [first stage] does not respond to fluid or mannitol load tests, fluid intake should be strictly controlled based on the measured urine output. The rise in serum creatinine or hematuria nitrogen levels and electrolyte concentrations can serve as criteria for dialysis treatment. Evidence suggests that supplementation with high-quality nutrition may help reduce the need for dialysis and lower morbidity and mortality rates. While appropriately adjusting fluid intake, daily supplementation with 30–35 kcal/kg of glucose and essential amino acids is recommended to correct or reduce the body's catabolic state.

Close monitoring of blood potassium levels and continuous electrocardiogram checks aid in the early detection of hyperkalemia. If hyperkalemia occurs, the following treatment measures can be taken:

① Intravenous infusion of sodium bicarbonate.

② Oral or rectal administration of the cation exchange resin Kayexalate (25–50 g) with sorbitol.

③ Intravenous drip of glucose and insulin.

④ Intravenous calcium supplementation to suppress myocardial excitability.

⑤ Peritoneal or hemodialysis if necessary to prevent or treat uremia, hyperkalemia, and fluid retention.

bubble_chart Prognosis

Most patients recover within 7 to 14 days, but kidney damage may persist, especially in elderly patients.