Acute kidney injury (AKI) is an abrupt and often reversible drop in the GFR leading to rise in s. BUN, SCr, and other metabolic wastes that are normal
(Art & science)
By: Fedaey Abbas (MD)
Abbreviations (read twice please):
o a.a: amino acids
o AB: antibiotics
o ACEi: angiotensin-converting enzyme inhibitors,
o AKI: Acute kidney injury
o AL (OH) 3: Aluminum hydroxide.
o AL: aluminum
o ALI: acute lung injury
o APO: Acute Pulmonary edema
o ARBs: angiotensin receptor blockers.
o ATN: acute tubular necrosis
o AUN: acute urate nephropathy
o BP: blood pressure
o BUN: blood urea nitrogen
o Ca+: calcium
o CIN: contrast-induced nephropathy
o CKD: chronic kidney disease,
o CO: cardiac output
o CO2: carbon dioxide.
o CVS: cardiovascular
o Dgx: Diagnosis
o DKA: diabetic ketoacidosis
o DX: Dialysis
o ED: emergency department
o ESKD: end-stage kidney disease,
o GFR: glomerular filtration rate
o GI: gastrointestinal
o GN: glomerulonephritis
o HCO3: bicarbonate
o HF: heart failure
o Hpt: Hypotension
o HV: hypervolemia
o HvL: hypovolemia
o Hyper-K+: Hyperkalemia
o Hyper-PO4: Hyperphosphatemia
o Hypo-PO4: hypophosphatemia.
o IV: intravenous
o KDIGO: Kidney Disease: Improving Global Outcomes
o LT: life-threatening
o LV: left ventricular
o M.acd: metabolic acidosis
o M.alK: metabolic alkalosis
o MR: mortality rate.
o NS: nephrotic syndrome
o NSAIDs: nonsteroidal anti-inflammatory drugs,
o P+: phosphorous
o PO4: phosphate
o Ptns: patients
o Rhbdlss: rhabdomyolysis
o RI: renal impairment
o RPGN: rapidly progressive GN
o RRT: renal replacement therapy
o SCr: S. creatinine
o SE: side effects
o Sms: symptoms
o Sns: signs
o STEMI: ST-elevation myocardial infarction.
o TLS: tumor lysis syndrome
o ttt: treatment
o U/S ultrasound
o UA: uric acid
o UF: ultrafiltration
o UO: urine output
o UTO: urinary tract obstruction
o VC: vasoconstriction
o VD: Vasodilatation
Acute kidney injury (AKI) is an abrupt and often reversible drop in the GFR leading to rise in s. BUN, SCr, and other metabolic wastes that are normally renally excreted. The initial evaluation of ptns with AKI and management of the major Sequelae of AKI will be assessed. Ptns with AKI that is recognized as crucial part of the medical practice need systematic evaluation for the current threats and the associated Sequelae, followed by severity assessment with eliminating the underlying cause. The KDIGO guide lines classified the severity of AKI from stage 1 (mild) to stage 3 (severe). Generally, the AKI Sequelae are more severe and LT with higher stages of AKI. However, all ptns with AKI are at risk for progression from milder AKI to more intense AKI. The initial steps of urgent management relied primarily upon whether the ptn is hospitalized or in an OPD ptn.
Evaluation of OPD ptn with AKI: In the OPD setting, initial evaluation of the ptn with AKI is directed at recognizing the ptn to the proper setting, e.g., the ED for more serious disease or LT electrolyte abnormalities.
ED referral: the following ptns should be referred to the ED:
o Stage 2 or 3 as per KDIGO criteria (see below).
o Stage 1 with unclear etiology, ptns with unknown duration or course of rising SCr, or not rapidly reversing AKI with simple interventions (e.g., IV volume or removing nephrotoxin).
o Stage 1 AKI with uncontrolled co-morbid disease (e.g., acute on chronic exacerbation of HF, DKA).
o Any case with lack of certainty in regard to the cause/course of AKI.
o AKI at any stage in a resource-limited OPD where primary evaluation (e.g., renal U/S) or interventions (e.g., IV fluids) requiring an ED referral.
Ptns who do NOT need referral to the ED
Indications for urgent nephrology referral: Ptns who do not need an ED referral and managed as an OPD should be referred for OPD nephrology consultation if:
o Initial intervention failed to correct the renal injury.
o GN is strong Dgx (e.g., AKI + hematuria/proteinuria syndrome).
o AKI seen as a complication of ttt of an unrelated disorder and future ttt relied upon nephrology practice (e.g., AKI related to chemotherapy).
Timing to obtain an OPD nephrology consultation is variable. Ptn with suspected GN Dgx should be seen by a nephrologist next 1-2 d.s. However, if the AKI is related to other etiologies, an initial assessment within a week seems to be reasonable. If urgent nephrology referral cannot be obtained, then ptn should be shifted to the ED. Moreover, ptns having history of recent hospitalization for assessment/management of AKI should also be revised by an OPD nephrologist for long-term follow-up & secondary prevention of AKI. This cohort of ptns are at an increasing risk for recurrent AKI.
Urgent RRT: The management of LT fluid & electrolyte alterations related to AKI should be commenced immediately. Sequelae of AKI requiring urgent RRT include the following:
o Urgent medical intoxications.
o Hyper-K+ >6.5 mEq/L, Hyper-K+ + Sms/Sns (i.e., cardiac conduction defects, weak muscles), or
o Hyper-K+ >5.5 mEq/L + current tissue breakdown (e.g., Rhbdlss) or current K+ absorption (e.g., severe GI bleeding).
o Sns of uremia, e.g., pericarditis, or unclear decline in ptn mentality.
o Severe MA (pH <7.1) + HV, unless acidosis can be rapidly corrected via managing underlying etiology (e.g., DKA)
Ptns with any of these Sequelae despite proper medical intervention generally need urgent RRT. However, as RRT cannot be urgently provided, these Ptns usually need medical support before commencing RRT.
Role of 200 & 200 & in 2 hours
HV + APO: Ptns presenting with AKI and with severe hypoxia due to APO often need urgent RRT. Certain groups of ptns may respond rapidly to a loop diuretic and may avoid RRT requirement. For oliguric/hemodynamically stable ptns, we use 80-200 mg of IV furosemide or equivalent dosing and monitor for a rise in UO. A UO of > 200 mL within 2 h.s of the furosemide dose is adequate. Lower dosage (e.g., 80 mg) with no adequate response, then increased dose (e.g., 200 mg) should be given with no delay. Ptns with poor response to diuretics must be prepared for RRT.
Dose strategy for diuretics in AKI have not been well-developed, so, cautious alertness to SE e.g., ototoxicity is required. Moreover, the main target of diuretics use is to control HV. There’s no evidence that diuretics administration impact the incidence or intensity of AKI. Diuretics’ action may also help classify the intensity of renal injury. Study: 326 AKI ptns, diuretics use was complicated with an increasing risk of MR or lack of recovery of kidney function. Lack of response to diuretics can be defined as the furosemide dose = 1 mg/mL of daily UO (e.g., 200 mL UO responding to 200 mg of furosemide = dosing equivalent ratio of 1 mg/mL). Ptns with a ratio of 1 or more on the day of seeing nephrology consultant had higher odds of MR or non-recovery as compared to lack of diuretics. In contrary, ptns with a dose ratio of < 1 may show no significant rise in risk. These data lead to the suggestion that continuous use of loop diuretics is not advised in ptns with no rise in UO and that the lack “diuretic responsiveness” may be a Sn of increasing intensity of AKI. Many ptns with AKI & HV that’s not severely enough to indicate an urgent RRT.
Severe Hyper-K+: Ptns with AKI having S. K+ >6.5 mEq/L or those with Sms/Sns of Hyper-K+ (i.e., cardiac conduction defects, weak muscles) must be urgently dialyzed (preferably with HDX), with added rapidly acting agents (i.e., insulin /glucose, IV Ca+) & GI K+ binders. Moreover, ptns with AKI & Hyper-K+ >5.5 mEq/L should be emergently dialyzed with a currently tissue breakdown (e.g., Rhbdlss) or currently absorbed K+ (e.g., severe GI bleeds).
LT uremic Sms: Uremic Sms can be observed in ptns with AKI. Ptns with AKI having seizures or intense pericardial effusion related to uremia should commence an urgent RRT. Ptns with less severe uremic manifestations, e.g., altered sensorium, can be also commonly managed via RRT.
Toxic exposure: DX for toxin exposures requiring extracorporeal clearance.
Subsequent management of AKI includes:
o Recognition of the etiologies of AKI
o Correcting reversible insults, e.g., Hpt, volume depletion, or UTO
o Eliminating the active insults to limit adding new injuries.
o Identifying & correction of the Sequelae requiring RRT at a later stages (if AKI does not resolve)
Elimination & avoiding potential insults
Medications: With diagnosed AKI, we hold certain medications e.g., NSAIDs, ACEi, ARBs, & nephrotoxic agents (e.g., aminoglycosides, amphotericin, tenofovir, nephrotoxic chemotherapy), at least in the acute AKI stage. However, an exception from this withdrawal are medications accused in AKI development but cannot be withdrawn (e.g., being required to manage LT states).
Drugs with renal clearance producing serious hazard effects if accumulated with AKI should also be withdrawn or have dose adjustment, even if they may not directly alter renal function (e.g., metformin, gabapentin, cefepime, morphine). If possible, ptn can be switched to an alternate agent that is not currently renally excreted. Therapeutic drug monitoring with assisting experienced pharmacist in dosing adjustment may be asked.
Dosing: All medications in AKI should be promptly revised for the proper dosage, as required, considering the presumed GFR. However, AKI ptn is usually not in stable setting and the eGFR derived from SCr) should NOT be utilized for dose adjustment, rather, we consider the trend in SCr over several readings to assess the degree of drop in GFR. It is essential to remember that medication dosing may be altered several times along the course of AKI according to the eGFR:
o If SCr is suddenly rising (or if only a single reading is available), the GFR should be considered 0 mL/min, & drugs should be adjusted according to this level.
o If SCr is improving, the eGFR based on SCr is likely underestimating the true GFR. So, medications should be adjusted to a GFR more than the calculated eGFR with daily dose correction according to the rate of improvement.
o If SCr became plateau leveling & stable for several days, SCr can be applied now to estimate the GFR (via estimating formula).
o Agents with a clear physiologic impact (e.g., a vasopressor), dose titration should be commenced to achieve the target clinical end-points.
The SCr level may not precisely reflecting the real GFR in un-stabilized ptns. If the SCr level is actively rising, the eGFR based upon the SCr will be overestimating the real GFR. On the other hand, if the SCr is declining, the eGFR will be underestimating the real GFR. To realize this unsteady state setting of SCr, a kinetic GFR evaluating formula may be used instead.
Hypotension (Hpt): Low systolic and/or diastolic BP related to any cause can induce or complicate AKI. Fast recognition, assessment, and management of Hpt largely depending upon the etiology of Hpt and is essential to alleviate the intensity of renal injury.
Iodinated contrast agents: After AKI has been diagnosed, intravascular iodinated contrast media should NOT be utilized unless it is urgently required for a LT management, e.g., ttt of STEMI, or for a critically diagnostic procedure, e.g., recognition of dissecting aorta. In such settings, the lowermost possible dosing of contrast media should be provided with the standard prophylactic precautions should be associated.
DX cannot be routinely advised to ameliorate the increasing risk of more AKI (i.e., for "contrast removal") after iodinated contrast-media testing with acute decline of the GFR. However, RRT may be required if renal function deteriorated owing to the associated iodinated CIN. In this setting, RRT indications are similar to that in ptn not receiving iodinated contrast media.
Volume assessment & management: Volume status should be evaluated in all ptns with AKI via clinical examination. Correcting volume depletion/overload (particularly if CO worsened) should be an essential target of AKI management. Any small amount of fluid overload can be complicated with an increased risk of MR & poor outcome, so, fluid repletion should be carefully administrated considering the net balance and preventing any overload.
Hypovolemic ptns: IV fluid repletion should be administered to ptns with past history of fluid losses (e.g., vomiting & diarrhea), a physical findings denoting HvL (Hpt & tachycardia), or oliguria. However, fluids repletion should be postponed in ptns with APO or with anuric ptns.
Resuscitation targets: The overall target of fluid repletion is to augment CO and correct tissue oxygenation in ptns with preload dependence or responding to volume expansion. Fluids administration in ptns who are NOT volume responsive is hazardous and should NOT be attempted. Fluid therapy should be directed to the physiological endpoints e.g.,
o Mean arterial BP, or
o Dynamic CO alterations (via invasive monitoring).
Properly reversed volume depletion in ptns with a pre-renal insult can correct renal perfusion and prohibit the progress to an ATN. With specific causes of AKI, maintaining tubular flow & UO is essential to excrete nephrotoxic agents, so, protecting renal tubules from more injury in certain cases e.g., Rhbdlss. Some ptns, e.g., liver cirrhosis or the NS, ptns may be apparently overloaded but have a real low effective circulating volume (intravascular volume depleted) and may respond with raising UO, improving GFR, with better hemodynamics after fluid repletion. For uncertain cases, centrally placed hemodynamic monitoring assessing the responsiveness to fluid therapy may help.
Fluids type/quantity: choosing type & quantity of fluid is primarily depending on the nature of the underlying disorders, clinical assessment, and the ptn's response to fluid repletion:
o For clinically proved HvL, give 1-3 liters of crystalloid (better buffered crystalloid) observing its clinical response. Volume responding ptns with better UO & improved GFR, & persistent HvL or cannot preserve fluid balance > continue isotonic fluids at 75 mL/h or more according to current losses.
o Volume status with difficult interpretation, e.g., elderly or ptns with low effective arterial blood volume > give small volume trial (< 1 liter) of an isotonic fluid. According to response, continuation of fluid therapy can be decided.
o Ptns not responding to fluid therapy with increased UO or a decline in SCr are unlikely volume depleted and are more likely to have ATN diagnosis or other intrinsic AKI e.g., RPGN or acute interstitial nephritis. Volume expansion in this setting (after testing trial) is prohibited.
o Acute pancreatitis, Rhbdlss, or TLS > more liberality in fluid repletion plans.
For all cases careful & repeated assessment and monitoring are crucial to optimize ttt, to augment benefits, and to limit harmful adverse events while providing IV fluid therapy. Colloid solutions are not advised for ttt of HvL in ptns with AKI.
Hypervolemic (HV) ptns: HV may be observed at initial clinical evaluation or seen due to extra fluid provided with deficient ability to clear Na+ & water. This is can be seen in ptns with sepsis while receiving an aggressive IV fluid repletion. Fluid balance is usually positive in ptns with ATN with critical illness due to mandated fluid supplies with administered AB, blood products, other IV agents, and nutrient supplements. The end result will be increasing volume expansion with impending and intolerant APO particularly with ALI that may be complicated with poor outcome. Less commonly, volume overload may be seen with primary LV/ RV dysfunction leading to AKI development (type 1 cardiorenal syndrome).
Role of diuretics: Diuretics may be utilized to alleviate HV with non-anuric AKI ptns. Loop diuretics are usually preferable for their great natriuretic action compared to thiazides. Loop diuretics dosage is inversely related to the GFR. So, high (may be maximal) dosing of diuretics may be required with falling GFR. For hospitalized AKI ptns, diuretics are usually administrated IV rather than oral route since the absorption of the orally given agents is disturbed in ptns with impaired intestinal perfusion & mobility and in ptns with edematous mucosa:
o For diuretic-naïve ptns, initial 80 mg IV furosemide can be given with assessment of response. Ptns on diuretic use before the AKI should be given a dose that is at least doubling their previous dosing.
o With no clear rise in UO within 2 h.s, we can double the initial doses (up to 200 mg single dose IV furosemide). Adding thiazides e.g., chlorothiazide (500-1000 mg IV) with furosemide may augment UO. Lacking of response to a 200 mg of IV furosemide, with or without a thiazides, may raise the need for RRT.
o Ptns responding to diuretics, repeat the doses to prevent HV with imminent renal function recovery. However, with response to diuretics, the UO may be too little to prevent worsened HV with higher obligatory intake. So, if improvement is not obvious, we usually avoid diuretic use to postpone RRT, as DX + UF provide the most efficacious tool for volume deloading in AKI ptns.
Role of RRT: RRT typically started for volume overloaded ptns with anuria for > 24 hs not responding to diuretics, or with little response to diuretics to prevent worsened HV due to higher obligated repletion. Added to alleviated volume overload, RRT may permit optimizing nutritional supplementations and to provide IV medication with no warning for deteriorated volume overload. However, the benefit of the early start of RRT for volume control still uncertain, despite the associated link of intensity of volume overload at RRT start and the MR.
Hyper-K+: control of Hyper-K+ is primarily depending on its severity, cause of the AKI (reversible or resistant), associated clinical sequelae (cardiac conduction defects), and the response of medical interference. All cases with Hyper-K+ should be on K+-restricted diet (< 2 g/d). Moreover, all K+-rich medications should be discouraged. Specified ttt of Hyper-K+ is aimed at: (1) opposing the membrane actions of K+, (2) pushing extracellular K+ inside the cells, or (3) clearing extra K+ outside the body.
o No need for DX, at least early, for mild Hyper-K+ & AKI related to a well-known, reversible causes (e.g., depleted volume or an ACEi/ARB). Holding ACEi/ARB, a low-K+ diet, volume supplies with/without diuretic (in euvolemic or hypovolemic ptns), or diuretic alone (in HV ptns). Repeated K+ level should be provided within 24-48 hs according to the level of Hyper-K+ and the expected response to therapeutic interventions.
o No need for DX, at least early, for ptns with AKI due to not rapidly reversible causes, e.g., ATN, and having Hyper-K+ that can be properly managed with medical intervention.
However, according to other variables (e.g., the timing of the day & staff availability), preparing for RRT, e.g., placing a DX catheter, are usually started for these ptns, as Hyper-K+ is likely to be recurrent unless kidney function recovered. This is particularly true for oliguric/anuric ptns, but therapeutic approach should be individualized for each ptn. Moreover, certain cohort of ptns with Hyper-K+ that is related to continuous efflux of intracellular K+ (Rhbdlss, compartment syndrome, TLS) should perform early RRT to attain sustained stability of K+.
Hyper-PO4: Restricted dietary P+ to <2 g/d is usually advised in all ptns with AKI, except those with Hypo-PO4. Despite the lack of necessary evidence to support this approach, typically, PO4 binders can be provided in AKI ptns with the following:
o PO4 level >5.5 mg/dL (1.8 mmol/L)
o Current enteral feeding (eating or tube feeding)
o Prolonged AKI (i.e., AKI is not currently reversible)
o Hyper-PO4 + severe hypo-Ca+, even if PO4 <6 mg/dL or if RRT is imminent
o Hyper-PO4 + continuous efflux of intracellular PO4 e.g., Rhbdlss & TLS
The choice of PO4 binder is depending on the level of the ionized Ca+ levels. If ionized Ca+ is diminished, Ca+-containing PO4 binder e.g., Ca+ acetate or Ca+ CO3 can be supplied to manage s. PO4 level, provided that ptns can take oral agents. If ionized Ca+ level is high, non-Ca+ PO4 binder, e.g., lanthanum CO3, sevelamer, or (AL (OH) 3), should be supplied. Among these ptns, non-Ca+ binders are preferable to prevent rises in the Ca+/ PO4 product. However, there’re no current data comparing outcome among ptns managed with different medications in the setting of AKI. Using Al (OH) 3 should be limited to few days to limit the accumulated AL. Despite the lack of evidence supporting this approach, the goal of PO4 binders is to preserve PO4 in its normal range with individual titration to achieve this target. There’re no reported data showing that therapy of acute Hyper-PO4 associating AKI can improve ptn outcome. Mild Hyper-PO4 (i.e., 4.5-5.5 mg/dL) related to AKI should NOT be treated.
Hypocalcemia: ttt of hypo-Ca+ usually depending on its acuity, severity, & finding of Sms. Hyper-PO4 should also be controlled in ptns with associated hypo-Ca+. Control of s. PO4 as with an oral PO4 binder is usually sufficient to correct s. Ca+. In the case of Hyper-PO4-induced hypo-Ca+, the dose of Ca+ supplements should be limited to alleviate Sms and not necessarily to normalize s.Ca+ levels that can increase the Ca+/PO4 product to a level that can induce Ca+ precipitation. Diagnosing hypo-Ca+ as well as its monitoring, s. ionized Ca+ should be assessed with the total s.Ca+ if measuring ionized Ca+ is feasible. Total s.Ca+ does not precisely reflecting the ionized Ca+ among ptns with decreased or higher s. albumin level, as Ca+ is usually bounding to albumin. Moreover, as binding of Ca+ to albumin is pH related, the amount of free Ca+ can be changed by acid-base alterations or by the fast control of these changes.
Hypo-Mg+ & hyper-Mg+: Ptns with hypo-Mg+ & RI should be managed cautiously via small dosing and repeated monitoring. Hyper-Mg+ may be seen in ptns with AKI considering the vital role offered by the kidney in Mg+ clearance. Severely, symptomatizing hyper-Mg+ is rare except in ptns managed with high dosing of IV Mg+, e.g., ladies with intense preeclampsia.
Hyperuricemia: Ptns with TLS can develop AKI as a result of severe elevations of UA & AUN. Less intense hyperuricemia seen in ptns without TLS is frequently seen in ptns with AKI owing to deficient kidney excretion of UA. The role of urate-decreasing agents in this scenario is uncertain.
Acid-base disturbance: Acid-base alterations are usually seen in ptns with AKI as a sequela or as a direct reflection of its underlying cause. MA is more commonly observed, despite M.alK can be also seen.
MA: We can commence RRT with oliguric/anuric AKI ptns with volume overload and severe MA (pH <7.1), unless this acidosis can be rapidly corrected by rapid correction of the underlying cause (e.g., DKA). However, ptns with AKI + severe MA and not overloaded with no other indications to initiate RRT, HCO3 may be given instead of RRT; a diuretic can be supplied in non-oliguric ptns to abort HV and to enhance acid clearance. Target S. HCO3 level is 20-22 mEq/L and the target pH is >7.2.
In non-dialyzed ptns, total magnitude of S. HCO3 that will be required can be assessed from the calculated HCO3 deficits. The rate of HCO3 infusion is relied on the intensity of acidosis and on the volume setting of the ptn. A reasonable protocol is to provide 3 ampules (= or 150 mEq) of Na+HCO3 in 1 L of 5 % dextrose with a rate according to acidosis severity and ability of the ptn to accommodate volume load. Oral Na+ HCO3 tablet or Na+ citrate sol. can also be administrated in ptns tolerating oral agents and having mild acidosis (HCO3 >18 mEq/L). HCO3 deficit calculations guiding the therapy and aiming at 50 % deficit replacement in the 1st 24 hs.
RRT is currently preferable to the IV HCO3 in HV ptns with decreased UO, as HCO3 may induce a large Na+ burden leading to worsened volume overload. Oliguric or anuric ptns with no HV, HCO3 therapy may also induce volume overload and should therefore be used cautiously. In ptns with AKI, HCO3 supply may be complicated with serious SE related to hypo- Ca+ & hypo-K+ development. HCO3 supplementation may induce dropping in the ionized or free Ca+ due to pH-dependent rise in Ca+ binding to albumin. The latter may worsen the Sms of hypocalcemia (e.g., tetany) as Sms of hypo-Ca+ is reflecting the ionized, not total, Ca+. As in ptns with no AKI, HCO3 could induce hypernatremia, rise in the partial pressure of pCO2 in ptns with circulatory/ventilation compromise, and raised intracranial tension in ptns with DKA.
Physiological setting: at pH of <7.1, acidemia may induce hemodynamic alterations related to:
1) Impaired LV contractility,
3) Arterial VD/VC, &
4) Impaired response to catecholamine action.
Decline in GFR is the main cause of MA in AKI ptns, despite other agents may also contribute, like increased produced organic acids e.g., in lactic acidosis seen with altered perfusion. This acid is normally cleared by the kidney is mostly produced by the daily metabolic production.
Metabolic alkalosis: M.alK with AKI can be seen in a minority of ptns e.g., ptns with milk-alkali syndrome, persistent vomiting, or nasogastric tubing suction. Ptns are mostly hypovolemic and their alkalosis can typically respond to IV Na+ chloride. Compensatory M.alK with no alkalemia can also be observed in ptns with underlying pulmonary diseases developing AKI.
Nutritional support: The target of nutritional support in critically ill AKI ptns is to provide necessary amounts of energy, protein, as well as other nutrients. Restrictions on K+, P+, & Na+ intake can be applicable in most AKI ptns. Considering the complexity of nutritional supplementations in such ptns and the individual requirements for each ptn, a nutrition consultation in hospitalized ptns with stage 3 AKI is advised for the best tailored prescription. Ptns with less advanced AKI stages, a required nutrient consultation should be individualized. With absent volume depletion, ptns with AKI on RRT or with impending need for RRT can be also advised with fluid restriction of 1-1.5 L/d. Nutritional supplementations are primarily related to the intensity of the underlying disorder, previous nutritional setting, and other co-morbidities.
Despite variabilities in requirements that are currently related to the underlying catabolic status, some experts consider that ptns may need almost 25-30 kcal/kg/d. Other clinicians, however, may consider that underfeeding may actually be a preferable approach, despite the lack of evidence on underfeeding in AKI. Wasted protein energy is commonly seen in critically ill AKI ptns that contributing to MR. Protein needs are increasing with the intensity of the underlying cause and with commencing RRT. Whilst non-DX ptns with only mild/moderate disease may require only 0.8-1.2 g/kg/d., critically ill ptns or ptns who starting RRT usually require 1.2-1.5 g/kg/d. or even more. The adequate nutrition supplementation to AKI ptns requiring RRT may urgently need parenteral or enteral nutritional support. For critically ill ptns with no AKI, most physicians consider that enteral nutrition should be preferred to parenteral nutrition if possible owing to:
o Lowered cost,
o Less frequent/severe Sequelae,
o Less mucosal permeability,
o More wound healing, &
o Less rate of infections.
For AKI ptns, sparse data concerned safety and efficacy of enteral feeding. One study: enteral nutrition-related outcome was compared in 247 consecutive ptns with enteral feeding: 114 on DX, 68 with AKI but not requiring DX, and 65 with normal renal function. Other than higher % of nasogastric tube block and higher gastric residual volume in ptns on DX, no difference detected in GI & mechanical Sequelae in the 3 g.s. The mean supplies non-protein calories & protein consumption in DX ptns = 23.4 kcal/kg & 0.92 g/kg, resp., with administration of parenteral a.a. for daily RRT. Few accepted reports evaluating the safety & efficacy of parenteral feeding in AKI ptns. Cochrane review: cannot declare the entire benefits of parenteral feeding on outcome and was limited by the poor quality of the current reports.
Evaluation for uremia: Non-urgent DX may be required for ptns with AKI of long duration with developed uremic Sms, even in absence of other indications mentioned above. Uremic Sns & Sms may include anorexia, nausea, vomiting, metallic tasting, and altered sensorium. Uremic findings e.g., asterixis & pericardial rub, may be also observed. Considering the non-specifity of the uremic Sms & Sns, excluding other causes is crucial before RRT can be commenced, particularly in absence of other indications. However, a pericardial rub/effusion is a robust indicator to initiate RRT. Daily evaluation for uremic manifestations is crucial until AKI corrected or the ptn maintained on RRT. Deciding to commence RRT according to one of these Sms facing some difficulty. This is particularly evident for critically ill ptns with neurological dysfunction that could be attributed to several etiologies. So, RRT start should be commenced with a clear target of assessment whether or not current uremic Sms can be improved with treatment. Several DX sessions are currently required to declare if Sms is resolving with RRT therapy.
Uremic Bleeding: AKI can induce qualitative platelet dysfunction that can induce hemorrhagic catastrophes that may be clinically manifested primarily by cutaneous bleeding, but GI bleeding can be also observed.
SCr, electrolytes, ionized Ca+, total S. Ca+, & PO4 should be assessed on a daily bases in stable ptns. The s. Ca+ & ionized Ca+ should be evaluated more frequently (twice/d.) in ptns requiring Ca+ or HCO3. S.K+ should be evaluated more frequently in ptns with raised K+ at presentation or were oliguric or with hemodynamic instability. In addition, careful monitoring of daily weight, fluid intake, & UO to evaluate daily fluid balance. Ptns with critical illness who’re incontinent or unable to assess UO due to altered mental status, an indwelling catheter may be placed for accurate assessment of UO. The drawbacks of an indwelling catheter may include catheter infection and must be balanced against the possible benefits in individual ptn. Ptns with moderately severe AKI should be properly monitored after discharge whatever the magnitude of their recovery, in order to prevent recurrence of AKI, progress into CKD, ESKD, & CVS events. These ptns should arrange at least a single nephrology OPD visit, if possible, to assure proper management after discharge. If not available, nephrology follow-up, ptns should be followed by their primary care physicians. Simple intervention at the follow-up appointment include monitored kidney recovery, medications adjustment, volume assessment, BP reading, dietary consultation, and ptn educative programs.
AKI in RIFLE vs KDIGO
Rise in SCr of ≥0.3 mg/dL within 48 hs OR ≥50% within 7 d.
OR: UO of <0.5 mL/kg/h./>6 hs
Risk (RIFLE) or
stage I (KDIGO)
Raised SCr 1.5 times baseline
OR: UO of <0.5 mL/kg/h./6-12 h.s
Rise in SCr of ≥0.3 mg/dL or 1.5-1.9 times baseline OR: UO of <0.5 mL/kg/h for 6-12 hs
Injury (RIFLE) or
stage II (KDIGO)
Raised SCr to 2 times baseline
OR: UO of <0.5 mL/kg/h for 12-24 h.s
Rise in SCr to 2.0-2.9 times baseline
OR: UO of <0.5 mL/kg/h for 12-24 hs
Failure (RIFLE) or
stage III (KDIGO)
Raised SCr to 3 times baseline
OR: Raised SCr >0.5 mg/dL to >4.0 mg/dL
OR: UO of <0.3 mL/kg/h/>24 h or anuria for >12 hs
OR: Start of RRT
Rise in SCr to ≥3.0 times baseline
OR: Rise in SCr of ≥0.3 mg/dL to ≥4.0 mg/dL
OR: UO of <0.3 mL/kg/h for ≥24 hs or anuria for ≥12 hs
OR: Start of RRT.
RRT for >4 wks
RRT for >3 mo
RIFLE: risk, injury, failure, loss, ESKD.