Early AKI diagnosis using the Stewart approach Maciel AT and Park M Table 1 - Traditional renal and physicochemical parameters in the evolution of AKI. Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 BUN (mg/dL) 15 Creatinine (mg/dL) V 0.89 SIDa (mEq/L) *, V 34.5 SIDu (mEq/L) # 48 SIG (mEq/L) *, V 1.7 Lactate (mEq/L)V 0.9 Phosphate (mg/dL) V 3.0 FeNa (%) 1.5 FeCl (%) 1.9 FeK (%) 17.2 Preceding 24-h --- diuresis (mL) 10 0.76 37.1 51 2.6 2.1 1.8 4.7 5.2 19.4 2440 13 0.90 39.5 145 4.5 3.1 2.1 1.8 1.6 17.6 1100 17 0.87 39.8 160 7.0 2.6 3.1 0.9 0.7 15.3 920 27 0.95 38.4 108 9.1 3.2 3.8 0.1 0.3 25.1 840 47 2.14 40.0 106 14.2 6.4 5.5 0.1 0.2 39.6 225 AKI: acute kidney injury; BUN: blood urea nitrogen; SIDa: apparent strong ion difference; SIDu: urinary strong ion difference; SIG: strong ion gap (unmeasured anions); FeNa, FeCl, and FeK: fractional excretion of sodium, chloride and potassium, respectively. Vmeasured in blood. *SIDa and SIG were calculated as previously reported (see reference 3). # SIDu was calculated as follows: urinary [Na+] + [K+] – [Cl-]. is a late diagnostic marker. In this case, increases in creatinine occurred simultaneously with overt multiple-organ failure, which limited the likelihood of effective intervention. Using the Acute Kidney Injury Network criteria (2), AKI diagnosis in this patient was possible on day 4 by considering urine output (AKIN stage 1 – data not shown). A delayed diagnosis of AKI stage 2 was possible only on day 6 using the creatinine criteria, and AKI stage 3 could be diagnosed using urine- output criteria on day 5. Interestingly, other variables exhibited daily trends that suggested that AKI was develop- ing before the major changes in creatinine levels occurred. First, relative decreases in urinary flow should be taken into Figure 1 - Daily changes in electrolyte levels in spot urine samples. 526 CLINICS 2012;67(5):525-526 account; in this case, daily decreases in urine output might have suggested AKI as early as day 2, although the levels remained within a ‘‘normal’’ range (.0.5 ml/kg/h). Daily simultaneous increases in BUN, unmeasured anions, and phosphate levels, even within the normal range, could also be useful in the diagnosis of a progressive impairment in renal function. It has been previously demonstrated that hyper- phosphatemia and an increased concentration of unmea- sured anions account for metabolic acidosis in AKI (3). Furthermore, a persistently high SIDu (well above plasmatic SID; Table 1) would not be expected in hyperchloremic acidosis, which is usually present after major crystalloid infusion, as occurred during surgery. It has also been previously suggested that high levels of SIDu are associated with renal failure in metabolic acidosis (4). Finally, abrupt decreases in NaU, ClU, and their respective fractional excretions, occurring in parallel with increases in KU and its fractional excretion between days 4 and 6, might also signal severe renal hemodynamic compromise with exacer- bated activity of the sympathetic and angiotensin system (a ‘‘pre-renal’’ pattern of AKI). These changes were probably part of a systemic inflammatory response, with microcircu- latory impairment that, if left untreated, would lead to multiple-organ failure and death. This ‘‘pre-renal’’ pattern of AKI has been previously shown in experimental hyperdy- namic sepsis (5). Cardiac output was not measured in this patient, but successive positive fluid balances argue against hypovolemia as the main cause of the urinary findings. In conclusion, the daily evaluation of changes in simple parameters such as consistent increases in serum phosphate levels, unmeasured anions, and KU, with decreases in NaU and ClU and a persistently high SIDu, could facilitate the early diagnosis of renal impairment before major decreases in urine output or increases in creatinine are observed. Even small alterations in these parameters might be a warning sign of ongoing renal and perhaps systemic hemodynamic impairment. AUTHOR CONTRIBUTIONS Maciel AT provided care to the patient, collected and analyzed the data, and wrote the manuscript. Park M provided care to the patient and collected the data. REFERENCES 1. Stewart PA. Modern Quantitative Acid-Base Chemistry. Can J Physiol Pharmacol. 1983;61(12):1444-61, http://dx.doi.org/10.1139/y83-207. 2. Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, et al. Acute Kidney Injury Network: Report Of An Initiative To Improve Outcomes In Acute Kidney Injury. Crit Care. 2007;11(2):R31, http:// dx.doi.org/10.1186/cc5713. 3. Rocktaeschel J, Morimatsu H, Uchino S, Goldsmith D, Poustie S, Story D, et al. Acid-Base Status Of Critically Ill Patients With Acute Renal Failure: Analysis Based On Stewart-Figge Methodology. Crit Care 2003;7(4):R60. 4. Moviat M, Terpstra AM, Van Der Hoeven JG, Pickkers P. Impaired Renal Function Is Associated With Greater Urinary Strong Ion Differences In Critically Ill Patients With Metabolic Acidosis. J Crit Care. 2011 (In Press). 5. Langenberg C, Wan L, Bagshaw SM, Egi M, May CN, Bellomo R. Urinary Biochemistry In Experimental Septic Acute Renal Failure. Nephrol Dial Transplant. 2006;21(12):3389-97, http://dx.doi.org/ 10.1093/ndt/gfl541.