ACUTE KIDNEY INJURY Flashcards
Q: When we say AKI, what structures in the kidney are affected?
A: This is a trick question. There are no affected structures of the kidney in AKI, YET. AKI is a clinical diagnosis, not a structural diagnosis. In acute stages, the structures are normal. If the condition persists, that’s the time structural damages will occur.
Q: What is the definition of AKI according to creatinine levels?
A: AKI is defined by any of the following:
1) An increase of >0.3mg/dL or of >50% developing over <48hrs
2) Urine volume < 0.5 mL/kg/h for 6 hours.
Q: What does the Rifle Criteria say about the reversibility of AKI?
A: In the Rifle Criteria, stages RIF (Risk, Injury, and Failure) are still reversible. Once you reach Loss, there may be complete loss of renal function lasting more than four weeks.
Q: What is the main difference between the RIFLE criteria and AKIN classification?
A: The RIFLE criteria include GFR criteria, while the AKIN classification does not. AKIN focuses only on serum creatinine and urine output.
Q: At what stage of AKIN is renal replacement therapy (RRT) typically indicated?
A: Renal replacement therapy (usually hemodialysis) is indicated in AKIN stage 3 or if the patient’s condition worsens.
Q: What defines Stage 1 AKI based on serum creatinine and urine output?
A: Serum creatinine 1.5 to 1.9 times baseline OR increase by ≥26 μmol/L (≥0.3 mg/dL); Urine output <0.5 mL/kg/h for 6-12 hours.
Q: What defines Stage 2 AKI based on serum creatinine and urine output?
A: Serum creatinine 2 to 2.9 times baseline; Urine output <0.5 mL/kg/h for ≥12 hours.
Q: What defines Stage 3 AKI based on serum creatinine and urine output?
A: Serum creatinine increase ≥3.0 times baseline OR increase to ≥354 μmol/L (≥4.0 mg/dL) OR initiation of RRT; Urine output <0.3 mL/kg/h for ≥24 hours or anuria for ≥12 hours.
Q: What is the duration criterion that differentiates AKI from CKD?
A: AKI is <3 months duration, while CKD is >3 months duration.
Q: What are some radiologic differences between AKI and CKD?
A: In CKD, renal size is smaller, cortical thickness is reduced (usually <1 cm), and echogenicity appears lighter (gray) compared to normal kidneys.
Q: How does the trend of serum creatinine differ between AKI and CKD?
A: In AKI, serum creatinine rises more precipitously and acutely. In CKD, the increase is gradual.
Q: What is the relationship between serum creatinine and GFR?
A: Serum creatinine is a late marker of kidney function. Significant GFR reduction (about 75% nephron loss) occurs before creatinine rises noticeably.
Q: What are potential causes of increased BUN without AKI?
A: Increased BUN can occur due to:
1) Increased protein intake
2) Gastrointestinal bleeding
3) Catabolic states
4) Corticosteroids or tetracycline use.
Q: What are potential causes of increased serum creatinine without AKI?
A: Causes include:
1) Inhibition of tubular creatinine secretion (e.g., trimethoprim, cimetidine)
2) Lab assay interference (e.g., cephalosporins, ketones)
3) Increased muscle activity.
Q: What are the key pathophysiological mechanisms involved in AKI?
A: AKI involves microvascular compartment changes, innate immunity activation, and acute tubular necrosis, leading to temporary, partial, or permanent GFR loss.
Q: What is an example of extrarenal factors causing AKI?
A: Hemodynamic alterations like decreased cardiac output, low blood pressure, and systemic proinflammatory conditions can initiate or exacerbate AKI.
Q: What is the main source of serum creatinine?
A: Serum creatinine primarily comes from muscle metabolism.
Q: What is the typical urine output threshold for diagnosing anuria?
A: Anuria is defined as urine output <400 mL in 12 hours or longer.
Q: What is the definition of AKI based on serum creatinine levels in RIFLE?
A: An increase of >50% developing over <7 days.
Q: What is the definition of AKI based on serum creatinine levels in AKIN?
A: An increase of ≥0.3 mg/dL or >50% developing over <48 hours.
Q: What is the definition of AKI based on serum creatinine levels in KDIGO?
A: An increase of ≥0.3 mg/dL developing over <48 hours, or an increase of >50% developing over <7 days.
Q: What is the definition of AKI based on urine output in RIFLE?
A: Urine output <0.5 mL/kg/hr for >6 hours.
Q: What is the definition of AKI based on urine output in AKIN?
A: Urine output <0.5 mL/kg/hr for >6 hours.
Q: What is the definition of AKI based on urine output in KDIGO?
A: Urine output <0.5 mL/kg/hr for >6 hours.
Q: What is the most common cause of AKI?
A: Prerenal azotemia.
Q: What causes the rise in serum creatinine (SCrea) or BUN in prerenal azotemia?
A: Inadequate renal plasma flow and intra-glomerular hydrostatic pressure to maintain GFR.
Q: What is the homeostatic response to low effective circulating volume or cardiac output in prerenal azotemia?
A: Renal vasoconstriction and salt/water reabsorption to conserve water and maintain perfusion to vital organs.
Q: What conditions impair renal autoregulation and increase the risk of prerenal azotemia?
A: Arteriosclerosis, hypertension, old age (hyalinosis of vessels), and drugs (e.g., NSAIDs, ACE inhibitors).
Q: Can prerenal azotemia occur in individuals without renal disease? Give an example.
A: Yes, for example, profuse diarrhea causing fluid loss and dehydration can lead to prerenal azotemia.
Q: What key findings can be expected in the history of a patient with prerenal azotemia?
A: History of GI losses (e.g., vomiting) or renal losses (e.g., polyuria), and medication use.
Q: What physical exam findings suggest prerenal azotemia?
A: Orthostatic hypotension, tachycardia, decreased JVP, poor skin turgor, and dry mucous membranes.
Q: What urinary findings are expected in prerenal azotemia?
A: Bland urine sediment (no structural changes), increased specific gravity, and the following indices: BUN/creatinine >20, FENa <1%, U/P creatinine >20, and FE Urea <35% (if diuretics used).
Q: Does prerenal azotemia involve parenchymal damage?
A: No, there is no parenchymal damage in prerenal azotemia.
Q: What happens if prerenal azotemia persists for a prolonged period?
A: It can lead to ischemic injury, resulting in acute tubular necrosis (ATN), which is an intrinsic form of AKI.
What is the effect of sepsis on the kidney in Sepsis-Induced AKI?
The effect is intrarenal, characterized by decreased GFR and decreased blood pressure.
What mechanisms contribute to decreased GFR in Sepsis-Induced AKI?
Generalized arterial vasodilatation via cytokines and excessive efferent arterial vasodilatation.
What hemodynamic effects of sepsis contribute to AKI?
Renal vasoconstriction via activation of SNS, RAAS, vasopressin, and endothelin.
What is the role of endothelial damage in Sepsis-Induced AKI?
It causes microvascular thrombosis, ROS, WBC adhesion, and migration, leading to renal tubule cell injury.
What is the glycocalyx, and how is it altered in sepsis?
A thin layer of glycosaminoglycans covering the endothelial surface, facilitating blood flow; in sepsis, it is altered, impairing interactions and causing endothelial dysfunction.
What are the main causes of nephrotoxic AKI?
Pharmacologic compounds, endogenous substances, environmental exposures, and toxins affecting all kidney structures.
What are the mechanisms of nephrotoxic AKI caused by contrast agents?
Tubular toxicity, intrarenal vasoconstriction, and tubular obstruction.
Which drugs are notorious for causing nephrotoxic AKI?
Amphotericin B, aminoglycosides, iodinated contrast agents, and myeloma light chains.
What endogenous toxins can cause nephrotoxic AKI?
Myoglobin, hemoglobin, uric acid, and myeloma light chains.
How does rhabdomyolysis lead to AKI?
Injured muscle cells release myoglobin, which precipitates in the kidney, causing intratubular obstruction and toxicity.
What is Ischemia-Associated AKI also known as?
Ischemic Acute Tubular Necrosis (ATN).
What part of the kidney is most vulnerable to ischemic damage in Ischemic ATN?
The outer medulla.
What are the clinical presentations of Contrast-Induced AKI?
Rise in serum creatinine 24–48 hours after exposure, peaking at 3–5 days, and resolving within a week.
What is a major risk factor for Contrast-Induced AKI?
Preexisting CKD, diabetes mellitus nephropathy, CHF, or multiple myeloma.
What are the mechanisms of injury in Contrast-Induced AKI?
Hypoxia in the renal medulla, ROS-induced cytotoxic damage, and tubule obstruction due to contrast precipitation.
What is the clinical management of Contrast-Induced AKI?
Monitor serum creatinine; creatinine begins to rise 24–48 hours post-exposure and peaks at 3–5 days.
What causes Acute Phosphate Nephrotoxicity?
Use of sodium phosphate as a laxative or orally.
What is the mechanism of Acute Phosphate Nephrotoxicity?
Severe increase in serum phosphorus combined with volume depletion leads to calcium-phosphate precipitation in the kidney.
What are the risk factors for Acute Phosphate Nephrotoxicity?
CKD, elderly age, female gender, volume depletion, and use of NSAIDs, ACEi/ARB, lithium, or diuretics.
What is the diagnostic method for Acute Phosphate Nephrotoxicity?
Kidney biopsy.
What are the five types of Cardiorenal Syndrome (CRS)?
Type 1: Acute CRS, Type 2: Chronic CRS, Type 3: Acute RCS, Type 4: Chronic RCS, Type 5: Secondary CRS.
What defines Acute CRS (Type 1)?
Acute worsening of cardiac function leading to decreased kidney function.
What defines Chronic CRS (Type 2)?
Long-term abnormality in cardiac function leading to decreased kidney function.
What defines Acute RCS (Type 3)?
Acute worsening of kidney function causing cardiac dysfunction.
What defines Chronic RCS (Type 4)?
Long-term abnormality in kidney function leading to cardiac disease.
What defines Secondary CRS (Type 5)?
Systemic conditions causing simultaneous dysfunction of the heart and kidney.
What is a common cause of AKI after surgery?
Postoperative AKI due to significant blood loss or intraoperative hypotension.
What is a common mechanism of AKI in burn or pancreatitis patients?
Diseases of the microvasculature leading to ischemia or thrombotic microangiopathies.
What are some examples of environmental nephrotoxins?
Glyphosate, paraquat, and 1,2-dibromo-3-chloropropane.
What is the cause of postrenal AKI?
Postrenal AKI occurs when the normally unidirectional flow of urine is acutely blocked either partially or totally, leading to increased retrograde hydrostatic pressure and interference with glomerular filtration.
What structures are involved in postrenal AKI?
Structures after the kidney: ureter, bladder, and prostate.
What is the effect of urinary tract obstruction on glomerular filtration rate (GFR)?
Obstruction increases retrograde hydrostatic pressure, leading to decreased GFR.
In postrenal AKI, how does retrograde pressure contribute to decreased GFR?
Retrograde pressure opposes downgradient flow, reducing GFR.
What is the prerequisite for developing postrenal AKI?
Bilateral obstruction or unilateral obstruction in a patient with one functioning kidney (e.g., bladder neck obstruction due to BPH or anticholinergic drugs).
What is a common urinary tract obstruction in men leading to postrenal AKI?
Bladder neck obstruction caused by benign prostatic hyperplasia (BPH).
How can surgical trauma cause postrenal AKI?
Surgical trauma can lead to ureteral ligation, which causes bilateral obstruction.
What are extrinsic causes of upper urinary tract obstruction in postrenal AKI?
Lymph nodes, tumors, fibrosis due to radiation, or ureteral ligation.
What intrinsic upper urinary tract conditions can lead to postrenal AKI?
Tuberculosis affecting the urinary tract or strictures in both ureters.
What is a key characteristic of lower urinary tract obstruction in postrenal AKI?
It can be a singular obstruction, such as in BPH or bladder neck obstruction.
What role does a kinked or blocked catheter play in postrenal AKI?
It can cause bilateral obstruction by blocking urine flow.
How does an abrupt increase in intratubular pressure affect the kidney in postrenal AKI?
It triggers afferent arterial vasodilatation, followed by intrarenal vasoconstriction.
What are common clinical features of postrenal AKI?
Abdominal and flank pain, palpable bladder, hematuria if stones are present.
What diagnostic tests are used for postrenal AKI?
Plain abdominal x-ray, renal ultrasonography, postvoid residual bladder volume, computed tomography, retrograde or antegrade pyelography.
What urinary findings suggest postrenal AKI?
Frequently normal urinalysis or hematuria if caused by stones or prostatic hypertrophy.
What is the effect of bilateral obstruction in the upper urinary tract?
It leads to decreased GFR and postrenal AKI.
How does neurogenic bladder contribute to postrenal AKI?
It causes functional obstruction at the lower urinary tract.
What is the normal body’s initial response to abrupt increases in intratubular pressures?
Afferent arterial vasodilatation.
What is a common cause of postrenal AKI in obstetric cases?
Surgical trauma causing ureteral ligation.
Why is catheter patency important in managing postrenal AKI?
A kinked or blocked catheter can lead to bilateral obstruction, worsening the condition.
