Dornfeld L, Narins R G
Urol Clin North Am. 1976 Jun;3(2):363-77.
The acute onset of oliguria and azotemia in the postoperative setting may be caused by pre-renal causes or intrinsic renal damage. The first step in arriving at a diagnosis is to review the history as noted above for clues regarding fluid balance, treatment with nephrotoxins, etc. The typical patient with prerenal azotemia will present with evidence of the recent onset of worsening of pre-existing cardiac disease, renal or gastrointestinal fluid loss, or the accumulation of acites, edema, or retroperitoneal fluid. In the absence of very recent diuretic therapy, he will be excreting a scant amount of concentrated (greater than 400 mOsm per L) sodium free (less than 10 to 20 mEq per L) urine. The serumBUN/Cr ratio is often greater than 15 to 20:1, and their urinary sediment will be bland. In an occasional patient in whom these studies give equivocal results, additional help may be obtained with measurements of central venous pressure (CVP) or pulmonary wedge pressure (PWP) and by noting their response to intravenous fluid loading. A rising CVP or PWP in the face of salt loading is, of course, evidence against prerenal azotemia. Patients with obstructive uropathies may be oligoanuric or polyuric-occasionally a characteristic alternating polyuria and oliguria is found (due to displacement of a stone or relief of edema). When oliguric their urine typically contains substantial amounts of sodium (greater than 20 mEq per L), is isotonic, and their OsmU:OsmP is les s than or equal to 1.2. Their urinary sediment will reflect the cause of their obstruction as noted above. A renal scan, ultrasound study, or infusion IVP are mandatory to rule out the possibility of obstructive uropathy. If these nonivasive studies are equivocal, one must consider doing a unilateral retrograde. The development of ATN usually occurs in the setting of hypotension, sepsis, dehydration, and with exposure to nephrotoxins. Most patients with be excreting scant amounts of isotonic urine containing more than 20 to 30 mEq per L of sodium. Their CrU:CrP is less than or equal to 20:1 and their urinary sediment reveals many epithelial cells and casts. Those patients with nonoliguric ATN have urine outputs which may exceed 2 liters per day. Despite this output they demonstrate a stepwise increase in serum urea and creatinine. Urine sodium and osmolality are not very helpful in this setting. Many such patients do have low (less than 20 mEg per L) urine sodium concentration and excrete isotonic urine.
术后出现少尿和氮质血症的急性发作可能由肾前性原因或肾实质损伤引起。做出诊断的第一步是回顾上述病史，寻找有关液体平衡、肾毒性药物治疗等方面的线索。典型的肾前性氮质血症患者会有证据表明，既往存在的心脏病近期病情恶化、肾或胃肠道液体丢失，或腹水、水肿或腹膜后液体蓄积。在近期未使用利尿剂的情况下，患者排出的尿液量很少且浓缩（每升大于400毫渗量），无钠（每升小于10至20毫当量）。血清尿素氮/肌酐比值通常大于15至20:1，尿沉渣正常。偶尔，这些检查结果不明确的患者，可通过测量中心静脉压（CVP）或肺楔压（PWP）并观察其对静脉补液的反应来获得更多帮助。在给予盐负荷时CVP或PWP升高，当然是肾前性氮质血症的反证。梗阻性尿路病患者可能少尿或多尿，偶尔会出现特征性的交替性多尿和少尿（由于结石移位或水肿缓解）。少尿时，其尿液通常含大量钠（每升大于20毫当量），为等渗尿，尿渗量/血渗量小于或等于1.2。尿沉渣将反映上述梗阻原因。必须进行肾扫描、超声检查或静脉肾盂造影以排除梗阻性尿路病的可能性。如果这些非侵入性检查结果不明确，则必须考虑进行单侧逆行造影。急性肾小管坏死通常发生在低血压、脓毒症、脱水以及接触肾毒性药物的情况下。大多数患者排出的等渗尿量很少，每升含钠超过20至30毫当量。其尿肌酐/血肌酐小于或等于20:1，尿沉渣可见许多上皮细胞和管型。非少尿型急性肾小管坏死患者的尿量可能每天超过2升。尽管有这样的尿量，但他们的血清尿素和肌酐仍呈逐步升高。在此情况下，尿钠和渗透压帮助不大。许多此类患者尿钠浓度低（每升小于20毫当量），排出等渗尿。
