06 - LAB 9 Acute Kidney Injury PDF

AHMED, REYES, ROBLES, SUBIJANO, SUGATAN, TOLENTINO | CLINICAL ASPECTS — LAB 1 ACUTE KIDNEY INJURY DESCRIPTION Acute kidne...

AHMED, REYES, ROBLES, SUBIJANO, SUGATAN, TOLENTINO | CLINICAL ASPECTS — LAB 1 ACUTE KIDNEY INJURY DESCRIPTION Acute kidney injury or AKI is a common and serious problem in clinical medicine. It is characterized by an abrupt reduction in kidney function. This results in an PATIENT’S CASE accumulation of nitrogenous waste products and other toxins. On October 7, 2024, Patient AB, a 61-year-old Filipino male (70kg and 165cm), was brought to the emergency room due to DEFINITION shortness of breath, chest pain and lower extremity edema. KIDNEY DISEASE IMPROVING GLOBAL OUTCOMES (2012) Upon arrival of the patient, the medical resident-on-duty Acute Kidney Injury (AKI) is defined by an abrupt decrease checked the vital signs and the results are as follows: in kidney function. It includes patients without actual damage to the kidney but with functional impairment Vital Signs Results relative to physiologic demand Blood Pressure 120/80 mmHg AKI has been defined by changes in kidney function, Pulse Rate 92 beats/min including serum creatinine (SCr) changes and urine output Respiratory Rate 40 breaths/min within 48 hours or 7 days O2 Saturation 88% o In the context of acute kidney injury (AKI), "acute" is Body Temperature 36.4 C emphasized by setting a timeframe for diagnosis of After the initial assessment, the patient's next of kin was AKI interviewed regarding Patient AB's past medical history and was ▪ The word "acute" refers to a sudden or rapid onset of kidney dysfunction. AKI is a condition where kidney function declines known to be a smoker and hypertensive and is currently on quickly, over hours to days. Unlike chronic kidney disease (CKD), Losartan 100mg od. He had no history of previous surgical which progresses slowly over months to years, AKI is typically a procedures and the patient has no known allergies. The patient reversible condition if addressed promptly. currently works in a manufacturing firm as a manager and his ETIOLOGY food intake is mainly fastfood meals due to the lack of time in PRERENAL his schedule. Results from decreased renal perfusion in the setting of The physician ordered a laboratory test to assess the patient's undamaged parenchymal tissue condition. Laboratory results are as follows: INTRINSIC Tests Results Result of structural damage to the kidney, most commonly Blood Urea Nitrogen 5.64 mmol/L the tubule from an ischemic or toxic insult Creatinine 139.82 mmol/L (1.58 mg/dL) POSTRENAL Urinalysis Few Caused by obstruction of urine flow downstream from the Tests Results kidney Hemoglobin 15.6 g/L Hematocrit 48% CONTINUUM OF IMPAIRED KIDNEY FUNCTION RBC 5.0x108uL WBC 6.2X103/mm3 Neutrophils 61% Lymphocytes 33% Monocytes 2.4% Eosinophil 3% STAB 3.9% Basophil 0.5% Platelets 411x10/mm3 The Acute Disease Quality Initiative (ADQI) which is a workgroup composed of experts in nephrology and critical care, proposed to further subclassify AKI into ULTRASOUND RESULTS those who recover within 48 hours of injury (rapid reversal of AKI) and those whose injury persists beyond 48 hours (persistent AKI). Acute kidney injury becomes acute Tests Results Impression kidney disease (AKD) if kidney function is impaired beyond 7 days, and can Right ultimately transition into CKD if the duration exceeds 90 days. 10.08x4.62x4.35 cm Both kidneys Kidney INTEGRATED APPROACH TO INTERPRET MEASURES OF are normal Left KIDNEY FUNCTION AND STRUCTURE FOR DIAGNOSIS OF 11.72x4.63x4.32 cm in size Kidney AKI, AKD, AND CKD Kidneys Right 0.5x0.5 cm cyst on Bilateral Kidney Small Kidney upper third region Diagnosis GFR/SCr Oliguria renal damage kidneys Left 0.2x0.5 cm cyst on cysts AKI ✓ ✓ Kidney lower third region Urinary Bladder wall is thickened and AKD ✓ ✓ the volume measures cystitis T/C cystitis CKD ✓ ✓ ✓ ✓ Bladder 48.07cc AKI – changes in GFR or SCr levels accompanied by oliguria Prostate Normal in AKD – changes in GFR or SCr levels and presence of kidney damage 4.02 x 3.01 x 3.34 cm Gland size CKD – changes in GFR/SCr levels, oliguria, kidney damage, and small kidneys  AHMED, REYES, ROBLES, SUBIJANO, SUGATAN, TOLENTINO | CLINICAL ASPECTS — LAB 2 CLASSIFICATION CRITERIA FOR AKI STAGING KDIGO AKIN RIFLE KDIGO/AKIN/RIFLE Stage SCr Stage SCr Category SCr and GFR Urine Output ≥1.5-1.9 times Increase 1.5-2-fold Increase in serum baseline or from baseline or creatinine x1.5 or 25% increase increase Serum creatinine Increase >2- to 3- x2 or 50% Increase >3-fold from Serum creatinine 4 mg/dL (354 μmol/L) (354 mmol/L) Anuria for (≥353.6 μmol/L) with an acute increase Stage 3 Failure with an acute rise ≥12 hours increase or of at least 0.5 mg/dL >0.5 mg/dL Stage 3 (44 μmol/l) or (44 mmol/L) Initiation of renal GFR decreased replacement therapy On RRT >75% or In patients 3 months disease The Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelines working group in 2012 proposed a staging system that shares many similarities with both RIFLE and AKIN. o KDIGO - Kidney Disease: Improving Global Outcomes o AKIN - Acute Kidney Injury Network o RIFLE - Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease The progression from Acute Kidney Injury (AKI) to Chronic Kidney Disease (CKD) is a significant clinical concern. While AKI is a condition of rapid onset that typically occurs over hours or days, CKD is a long-term, progressive loss of kidney function that develops over months or years. AKI is a complex and multifactorial condition, and its treatment depends on the underlying cause. Whether the cause is reduced renal perfusion, direct kidney tissue damage, or urinary tract obstruction, early identification and intervention are critical to preventing long-term kidney damage and improving patient outcomes.  AHMED, REYES, ROBLES, SUBIJANO, SUGATAN, TOLENTINO | CLINICAL ASPECTS — LAB 3 PATHOPHYSIOLOGY OF AKI INJURY (ISCHEMIC OR TOXIC) RESULTS IN A number of pathophysiological mechanisms can contribute Rapid loss of cytoskeletal integrity and cell polarity to AKI following an ischemic or toxic insult Mislocalization of adhesion molecules & other membrane o Alterations in renal perfusion resulting from loss of proteins (Na+-K+ ATPase, β-integrins) autoregulation and increased renal vasoconstriction o Tubular dysfunction and cell death by apoptosis and Shedding of proximal tubule brush border necrosis Apoptosis and necrosis o Desquamation of viable & dead (tubular) cells SEVERE INJURY contributing to intratubular obstruction ▪ Intraluminal tubular obstruction may be due to the Viable and nonviable cells are desquamated, leaving development of obstructive casts leading to regions where basement membrane remains as the only tubular backleak barrier between filtrate and peritubular interstitium o Metabolic alterations resulting in transport Backleak of filtrate, especially when pressure in the tubule abnormalities that can lead to abnormalities of is increased due to intratubular obstruction resulting from tubuloglomerular balance cell debris in the lumen interacting with proteins (e.g. o Local production of inflammatory mediators resulting in fibronectin) that enter the lumen interstitial inflammation, and vascular congestion Generation of inflammatory & vasoactive mediators, which leading to small vessel obstruction and local ischemia can act on the vasculature to worsen the vasoconstriction (may be seen in septic patients) and inflammation PATHOPHYSIOLOGY OF AKI AT CELLULAR LEVEL RESULT AND REPAIR Impairment of kidney function over days to weeks result in retention of nitrogenous and other waste products normally cleared by kidneys Kidney efficiently restores cells lost owing to an ischemic or toxic insult resulting in cell death o Increasing recognition of longer-term detrimental effects of even brief periods of AKI  AHMED, REYES, ROBLES, SUBIJANO, SUGATAN, TOLENTINO | CLINICAL ASPECTS — LAB 4 PATHOPHYSIOLOGY OF PRE-RENAL AKI Activation of baroreceptors (arterial & cardiac) → triggers neural and humoral responses to Hypovolemia restore blood volume & arterial pressure Glomerular perfusion, ultrafiltration pressure, & filtration rate are preserved through: (1) afferent arteriolar vasodilation through a myogenic reflex (autoregulation) Mild Hypoperfusion (2) biosynthesis of vasodilator prostaglandin dilates afferent arterioles (3) efferent arteriolar constriction due to stimulation of angiotensin II (AII) Decline in GFR caused by the failure to increase the post glomerular vascular resistance because Severe Hypoperfusion of the already high levels of AII Drugs Interfering with Renal NSAIDS Contraindicated in volume depletion Adaptive Responses ACEIs Contraindicated in bilateral renal artery stenosis PATHOPHYSIOLOGY OF INTRINSIC AKI (INTRINSIC RENAL AZOTEMIA) Patients are subject to factors known to cause ATN (hypotension, ischemia, sepsis, nephrotoxins) but have not yet developed overt parenchymal injury Preventable phase Initiation Ischemic injury is most prominent in the: (1) terminal medullary portion of the proximal tubule (S3 segment, pars recta) (2) medullary portion of the thick ascending limb of the loop of Henle Continuous ischemic injury and inflammation due to endothelial damage resulting to vascular Extension Ischemic congestion AKI GFR stabilizes at its nadir (5-10 mL/min) Urine output at its lowest, uremic complications arise GFR remains low due to persistent intrarenal vasoconstriction & medullary ischemia triggered by: Maintenance (1) dysregulated release of vasoactive mediators from injured endothelial cells (2) congestion of medullary blood vessels (3) reperfusion injury induced by ROS and inflammatory mediators (4) epithelial cell injury through tubuloglomerular feedback Recovery Repair and regeneration of renal parenchymal cells particularly tubular epithelial cells Contrast Acute onset (within 24-48 hours) but reversible rise in BUN & creatinine levels (peak at 3-5 days; Nephropathy resolution within 1 week) Induced by antibiotics and anti-cancer drugs Direct Toxicity Aminoglycosides even at therapeutic levels to Tubule Amphotericin B: dose-related AKI Cisplatin/Carboplatin: provoke AKI after 7-10 days of exposure Nephrotoxic AKI Calcium: hypercalcemia → intrarenal vasoconstriction → ↓ GFR; Ca phosphate deposition → tubular obstruction Myoglobin and Hemoglobin: toxic effect on tubule epithelial cells promoting intrarenal oxidative Endogenous stress & intratubular cast formation Nephrotoxins Myeloma light chains (Myeloma Cast Nephropathy): intratubular casts containing filtered immunoglobulin light chains including Tamm-Horsfall protein Uric Acid/Oxalate: complicates treatment of lymphoproliferative or myeloproliferative disorders PATHOPHYSIOLOGY OF POST-RENAL AKI Early stages of obstruction (hours to days): continued glomerular filtration → increased intraluminal pressure upstream to the site of obstruction Late stages: gradual distention of the proximal ureter, renal pelvis, and calyces → fall in GFR → acute obstruction Acute obstruction: initially associated with modest increase in RBF followed by arteriolar vasoconstriction → further decrease in GFR After the acute onset of obstruction, GFR declines progressively, but it does not fall to zero  AHMED, REYES, ROBLES, SUBIJANO, SUGATAN, TOLENTINO | CLINICAL ASPECTS — LAB 5 TYPES OF AKI HISTORY FINDINGS PHYSICAL EXAMINATION FINDINGS Volume loss (e.g. history of vomiting, diarrhea, diuretic overuse, Weight loss, orthostatic hypotension, and hemorrhage, burns) tachycardia Pre-renal Thirst and reduced fluid intake Poor skin turgor AKI Dilated neck veins, S3 heart sound, Cardiac Disease pulmonary rales, peripheral edema Liver Disease Ascites, caput medusae, spider angiomas History of receiving nephrotoxic medications (including Acute over the counter, illicit, and herbal), hypotension, Muscle tenderness, compartment Intrinsic Renal Tubular trauma, or myalgias suggesting rhabdomyolysis, recent syndrome, assessment of volume status AKI Necrosis exposure to radiographic contrast agents Lupus, systemic sclerosis, rash, arthritis, uveitis, weight Periorbital, sacral, and lower-extremity Glomerular loss, fatigue, hepatitis C virus infection, HIV infection, edema; rash oral/nasal ulcers hematuria, foamy urine, cough, sinusitis, hemoptysis Medication use (e.g. antibiotics, proton pump Interstitial Fever, drug-related rash inhibitors), rash, arthralgias, fever, infectious illness Nephrotic syndrome, trauma, flank pain, Livedo reticularis, fundoscopic Vascular anticoagulation (atheroembolic disease), vessel examination (showing malignant catheterization, or vascular surgery hypertension), abdominal bruits Post-renal Urinary urgency or hesitancy, gross hematuria, polyuria, stones, Bladder distention, pelvic mass, prostate AKI medications, cancer enlargement MANIFESTATIONS SYMPTOMS CONSISTENT WITH FLUID OVERLOAD PATIENT PRESENTATION AND INITIAL ASSESSMENT Shortness of breath Lower extremity edema PATIENT PROFILE Chest pain 61-year-old Filipino male, 70 kg, 165 cm Symptoms such as shortness of breath and lower extremity edema can indicate fluid CHIEF COMPLAINTS retention, a common findings in AKI cases due to the kidneys’ reduced ability to regulate fluid balance. When the kidneys' ability to excrete excess fluid is impaired, Shortness of breath it leads to fluid accumulation in the body. When this fluid backs up into the lungs Chest pain (pulmonary edema), it causes chest pain as experienced by patient AB. Lower extremity edema DIAGNOSTIC IMAGING FINDINGS SUPPORTING AKI VITAL SIGNS ABNORMALITIES KIDNEY ULTRASOUND Vital Signs Results Normal Range Tests Results Impression Respiratory Rate 40 breaths/min 12-20 breaths/min Right 02 Saturation 88% 95% - 100% 10.08x4.62x4.35 cm Both kidneys Kidney are normal The vital signs presents significant abnormalities, including a respiratory rate of 40 Left 11.72x4.63x4.32 cm in size breaths per minute, which is indicative of tachypnea and an oxygen saturation of Kidney 88%, suggesting hypoxemia. Kidneys Right 0.5x0.5 cm cyst on AKI EVIDENCE Kidney upper third region Bilateral renal Left 0.2x0.5 cm cyst on cysts ELEVATED CREATININE LEVEL Kidney lower third region Test Results Normal Range Although the kidneys are of normal size, both kidneys have small cysts, which may Blood Urea not be directly responsible for AKI but should be noted as incidental findings that 5.64 mmol/L 2.1 - 8.5 mmol/L Nitrogen may exacerbate renal impairment. 61.9 - 114.9 mmol/L URINARY BLADDER ULTRASOUND 139.82 mmol/L Creatinine (0.7 - 1.3 mg/dL) (1.58 mg/dL) Tests Results Impression for MEN Bladder wall is thickened and The patient has showed an elevated creatinine level at 139.82 mmol/L (1.58 Urinary mg/dL). Without baseline data, we cannot ascertain a recent increase, but a value the volume measures cystitis T/C cystitis Bladder this high is a significant marker for kidney impairment, especially in the absence of 48.07cc chronic kidney disease (CKD) history. While the patient’s blood urea nitrogen is 5.64 mmol/L, which is within the normal range, it still suggests impaired kidney A thickened bladder wall and reduced volume suggest cystitis. This can potentially function when considered alongside the creatinine levels. contribute to urinary retention or obstructive uropathy, which are risk factors for AKI if not managed properly.  AHMED, REYES, ROBLES, SUBIJANO, SUGATAN, TOLENTINO | CLINICAL ASPECTS — LAB 6 NUTRITIONAL REQUIREMENT CATEGORY GUIDELINE Target: 25–30 kcal/kg/day for critically ill patients with AKI Fat intake: approximately 30-40% of total energy depending on patient’s needs Energy Requirements Carbohydrate intake: 50-60% of total calories Individualization: Adjust according to patient factors such as comorbidities, metabolic stress level, body composition, and whether the patient is on renal replacement therapy (RRT) Non-dialysis AKI: 0.8–1 g/kg/day to prevent excessive protein loss without overloading the kidneys Protein Intermittent Hemodialysis (IHD): 1.2–1.5 g/kg/day to compensate for protein loss during dialysis sessions Requirements Continuous Renal Replacement Therapy (CRRT): 1.5–2.5 g/kg/day, given the higher protein losses in CRRT Potassium and Phosphorus: Closely monitor and adjust to prevent accumulation, especially in patients not on dialysis Electrolyte Sodium: Limit sodium intake to help avoid fluid overload; specific restrictions depend on volume status and Management RRT use Calcium and Magnesium: Monitor levels frequently, as RRT can alter their levels; adjust as needed Fluid Intake: Adjust to the patient’s volume status, particularly in fluid overload or oliguria (low urine output) Fluid Management Volume Control: Monitor fluid balance closely, especially in patients on parenteral nutrition (PN), to prevent overload Enteral Nutrition (EN): Preferred route when the gastrointestinal tract is functional, supporting gut integrity and immune function Route of Feeding Parenteral Nutrition (PN): Use only when EN is not feasible or contraindicated; adjust the formula to control fluid and electrolyte levels. PN formulations should be tailored to AKI patients to avoid complications Trace Elements: Monitor and potentially supplement elements like zinc, selenium, and copper, particularly in Micronutrient patients on CRRT, as losses may be significant Supplementation Vitamins: Supplement water-soluble vitamins (especially vitamin B and vitamin C) due to losses during RRT; consider daily requirements based on patient’s metabolic needs and RRT modality Regular Assessments: Continuously evaluate nutritional, metabolic, and renal parameters to adapt nutrition support to the patient’s changing needs Monitoring and Adaptation to RRT Changes: Adjust protein and electrolyte intake based on whether the patient is on IHD or Adjustment CRRT and the frequency of dialysis Adjust for Metabolic Stress: Monitor markers of metabolic stress (e.g. urea, creatinine) to ensure nutrition support does not exacerbate the patient’s condition MANAGEMENT PHARMACOLOGIC MANAGEMENT SYMPTOM MEDICATION MECHANISM OF ACTION SIDE EFFECTS Furosemide 20-80 mg PO once Lower Extremity daily; may be increased by 20-40 Loop diuretic that inhibits Na-KCl Dehydration and electrolyte Edema mg q6-8hr; not to exceed 600 cotransporters imbalance mg/day Angiotensin II receptor blocker that Continue Losartan 100 mg OD as competitively and reversibly inhibits Pain in joints or muscles, nausea hypertensive medication and for its Hypertension angiotensin II from attaching to the AT1 and vomiting, dizziness, and kidney protection but dose may be receptor in tissues such as the adrenal headache lowered according to renal function gland and vascular smooth muscle NON-PHARMACOLOGIC MANAGEMENT INDICATION PROCEDURE 88% oxygen saturation Supplemental oxygen until patient is stable and oxygen saturation is above 95% Aspiration and Sclerotherapy Bilateral renal cyst Bilateral renal cysts can be caused by injury to the kidneys. This procedure is done through an insertion of a needle under the skin in order to puncture and drain the fluid in cyst. In some cases, a special solution is injected in the cyst to make it less likely to be filled again  AHMED, REYES, ROBLES, SUBIJANO, SUGATAN, TOLENTINO | CLINICAL ASPECTS — LAB 7 PHARMACIST RECOMMENDATION CATEGORY RECOMMENDATION RATIONALE Continue Losartan but monitor renal function ARBs like Losartan reduce proteinuria but may need closely; consider dose adjustment if renal function adjustment based on kidney function and potassium levels worsens Avoid NSAIDs and any potentially nephrotoxic NSAIDs can further impair renal function and contribute agents and educate to avoid them without to AKD progression Medication Review consulting Recommend Sodium Bicarbonate only when lab Sodium Bicarbonate can correct metabolic acidosis, which results indicate metabolic acidosis is associated with AKI Recommend Nitrofurantoin 100 mg PO twice daily Nitrofurantoin is effective and indicated as first line for for 5-7 days for cystitis of the patient, if eGFR >30 male with uncomplicated cystitis if renal function is mL/min sufficient AKI can lead to electrolyte imbalances (such as Recommend requesting electrolyte levels of hyperkalemia and hyponatremia), which can worsen the potassium and sodium symptoms of the patient Laboratory Test eGFR can provide a more accurate assessment of renal Request Recommend calculating the eGFR function Detects early signs of kidney damage and quantifies Recommend urinary protein screening protein loss Recommend and advice the patient on a target Hypertension Maintaining BP can slow CKD progression and reduce Blood Pressure of