Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Kidney Lect 17
Acute Kidney Injury
| Question | Answer |
|---|---|
| loss of renal function, as assessed by glomerular filtration rate (GFR), over a period of hours to days | Acute kidney injury |
| The hallmark of acute kidney injury | retention of nitrogenous waste products in the blood. This is often, but not always, accompanied by a reduction in urine volume. |
| Acute renal failure (ARF) | older term for AKI; now generally reserved for severe AKI requiring renal replacement therapy |
| Azotemia | the accumulation of nitrogenous waste products (e.g., urea, creatinine) in the blood |
| Uremia: definition + symptoms | the clinical syndrome of symptomatic renal failure: anorexia, nausea, vomiting, muscle cramps, restless legs, sleep disorders, asterixis, mental status changes, seizures, fluid and electrolyte disturbances, anemia, platelet dysfunction and pericarditis. |
| Oliguria: defintion + threshold | literally, low urine volume. This is usually defined as a 24-hour urine volume of less than 400 to 500 mL. This volume represents the minimal urine volume required to excrete the obligate daily solute load at a maximal urinary concentration. |
| Anuria | literally, absence of urine. This is usually defined as a 24-hour urine volume of less than 100 mL. |
| primary clinical manifestation of acute kidney injury is ... | accumulation of nitrogenous waste products in the blood – in particular urea (measured as blood urea nitrogen, BUN) and creatinine (AZOTEMIA); usually asymptomatic initially |
| Can you estimate the GFR from the serum concentration of urea and creatinine in acute kidney injury? | NO; In acute kidney injury, the concentrations of urea and creatinine are not necessarily in steady state. It is therefore not possible to estimate glomerular filtration rate from the serum concentrations of these solutes. |
| What electrolyte and water imbalances are seen in acute kidney injury? | Sodium + water retention (expanded extracell volume + volume overload-->edema + pulmonary edema); decreased excretion of K, H, and PO4-->spike in serume concentration |
| Differential diagnosis of Azotemia | Not all acute elevations of BUN/creatinine due to AKI; UREA+: protein loading, GI bleeding, catabolic steroids, and tetracycline. CREATININE+: due to inhibition of tubular secretion of creatinine |
| How can the concentration of urea in the blood rise despite preserved GFR? | + urea generation from protein loading (protein is metabolized to urea), GI bleeding (an endogenous protein load), catabolic steroids (glucocorticoids) which increase protein catabolism and tetracycline antibiotics ( inhibit protein synthesis). |
| How can the concentration of creatinine in the blood rise despite preserved GFR? | inhibition of tubular secretion of creatinine (cimetidine or trimethoprim) or as the result of interference with colorimetric creatinine assays by medications such as cefoxitin, flucytosine (an anti-fungal drug) or in ketotic states by acetoacetate. |
| What are the etiologies of acute kidney injury? | heterogenous syndrome resulting from many disparate etiologies. Categorized as: prerenal, intrinsic AKI, posternal AKI |
| ** Pathophysiology of Prerenal Acute Kidney Injury (prerenal azotemia) | Decreased renal perfusion->reduction in GFR; NO histologic changes-just hemodynamics->increased AII production+prostaglandins->maintained GFR, decreased FF->further changes cannot be compesated->GFR falls, Na+ & urea reabsorbed->increased BUN:creatinine |
| What are the clinical settings in which prerenal acute kidney injury occurs? | True volume depletion, decreased effective blood volume, states of renal vasoconstriction |
| How can hypercalcemia result in prerenal AKI? | Hypercalcimea-->renal vasoconstriction |
| How can NSAIDs lead to prerenal AKI? | inhibit afferent arteriolar dilation --> no opposition to AII --> marked decrease in renal plasma flow + glomerular capillary pressure in states associated with increased angiotensin 2 production |
| Hepatorenal syndrome | syndrome of intense renal vasoconstriction seen in advanced liver disease; does not reverse with intravascular volume expansion (unlike other forms of prerenal azotemia); reversed with liver transplant; high mortality without transplant (~50% in 2 weeks) |
| What are common findings in the history of prerenal syndrome? | Acute volume loss (vomiting, diarrhea, acute blood loss), decompensated CHF, liver disease or acute infection; recent history of diuretic; intake and output records and changes should be reviewed; symptoms: thirst, orthostatic symptoms |
| What are the typical physical exam findings in prerenal syndrome? | hypotension, tachycardia, orthostatic changes in pulse + blood pressure, decreased skin turgor, dryness of mucous membranes + axillae; true volume depletion or effective blood volume depletion symptoms |
| What are the lab findings in pre-renal AKI? | BUN:creatinine > 20:1 (reflects passive urea reabsorption from tubule due to decreased tubular fluid flow rate); oliguria; concentrated urine; increased renal tubular Na+ reabsorption; bland urine sediment |
| What BUN:creatinine ratio do you see in pre-renal AKI? | BUN:creatinine > 20:1 ; reflects passive urea reabsorption from tubule due to decreased tubular fluid flow rate |
| Oliguria in pre-renal AKI | (<500 mL/24 hours; may not be non-oliguric) |
| Urine osmolality + SG values in pre-renal syndrome | Concentrated urine (>700 mmol/L osmolality + SG > 1.020) |
| Urine Na+ values in pre-renal syndrome | Evidence of increased renal tubular Na+ reabsorption (urine volume <20 mmol/L) and fraction excretion of N+ <0.01 |
| Fractional Excretion of Sodium (FENa) | index of renal tubular sodium reabsorption that may be used to help differentiate between etiologies of acute kidney injury; FENa = excreted Na / filtered Na --> FENa = (UNa / PNa)/(U Cr/P Cr) |
| In oliguria + acute AKI, how do you differentiate between prerenal state and ATN? What lab value/calculation can help you distinguish between the two? | Prerenal: FENa < 0.01 (1%) while in ATN, FENa >0.02 (2%); there are multiple etiologies that can explain Na+ fractional excretion <0.01, however! |
| How do you treat pre-renal azotemia? | 1) correction of volume deficits (administer crystalloid solutions) 2) discontinue diuretics 3) discontinue hemodynamically altering drugs (NSAIDs, ACEi's, ARBs); optimize Cardiac function (ionotropes + vasodilators) |
| Postrenal acute kidney injury: definition, hallmark | aka obstructive uropathy; Postrenal acute kidney injury results from partial or complete obstruction of the urinary tract at any level between the renal pelvis and the urethral meatus; Hallmark: hydronehrosis (dilation of renal collecting system) |
| Obstructive uropathy: The level of obstruction is classified as upper tract when it is ____ or lower tract when it is at ____. | above the level of the urinary bladder (e.g., ureters or renal pelvis); the level of the bladder outlet or urethra |
| In upper tract obstruction, patients will have ____ serum creatinine due to... | normal or minimally elevated; due to continue function of the contralateral kidney (for upper tract to cause AKI, obstruction must be bilateral) |
| Complete obstruction results in ____. Partial obstruction-->urine flow may be... | anuria; normal, decreased (oliguria), increased (polyuria), or may fluctuate between polyuria and oliguria. |
| Postrenal acute kidney injury: pathophysiology | obstruction->increase intratubular pressure->hydrostatic pressure in bowman's capsule increased->RPF increases initially (raising capillary pressure)-->fall in GFR-->decline in RPF->GRF down->GFR decreased even as tubular pressure returns to normal |
| What are the possible etiologies for upper tract obstruction (intrinsic)? | nephrolithiasis, papillary necrosis, blood clot, transitional cell carcinoma |
| What are the possible etiologies for upper tract obstrucion (extrinsic)? | retroperitoneal or pelvic malignancy, retroperitoneal adenopathy, retroperitoneal fibrosis, endometriosis, abdominal aortic aneurysm |
| What are the possible etiologies for lower tract obstruction? | benign prostatic hypertrophy, prostate cancer, transitional cell carcinoma, urethral stricture, bladder stones, blood clots, neurogenic bladder |
| What is the typical history of a patient with postrenal AKI? | Frequently present without complaints; may have anuria, polyuria, or widely fluctuating urine volume; classic: urinary frequency, urgency, intermittency, hesitancy, nocturia, and incomplete voiding; upper tract->flank pain; hematuria |
| What are the findings on physical exam of patients with postrenal AKI? | may present with a distended bladder, palpable as a suprapubic mass. Other important findings may include prostatic enlargement, pelvic masses and adenopathy. |
| What are the laboratory findings of patients with postrenal AKI? | a.BUN:creatinine ratio – often > 20:1, (variable) b.Urine sediment – often unremarkable; microscopic hematuria (without RBC casts) may be present. Crystaluria may be seen in patients with nephrolithiasis c.Urine chemistries – variable and non-diagnosti |
| What diagnostic studies should be done to diagnose patients with postrenal AKI? | postvoidal residual bladder volume (>100 mL consistent with voiding dysfunction/lower tract obstruction); radiological studies (renal ultrasound, CT scan, nuclear medicine excretory program, retrograde pyelography, antegrade nephrostogram |
| functional test; may be used to define if urinary tract dilatation is due to obstruction | nuclear medicine excretory program |
| – invasive study; may be accompanied by placement of ureteral stent for treatment | retrograde pyelography |
| Best initial study for identifying kidney stones | CT scan |
| usual initial imaging study | renal ultrasound |
| invasive study; usually accompanied by placement of percutaneous nephrostomy for treatment | antegrade nephrostogram |
| Treatment of postrenal AKI | mechanical relief of obstruction: lower tract (bladder catheter), upper tract (ureteral stents or percutaneous nephrostomies; both kidneys need to be decompressed to provide optimal long term benefit |
| Prognosis of postrenal AKI | if obstruction relieved within 1-2 weeks, functional recovery excellent; if longer than that, chronic kidney injury likely |
| Relief of urinary obstruction may be accompanied by a ___. As a result, patients need to be monitored closely to ensure that they do not develop volume depletion and intravenous fluid administration is often required | post-obstructive diuresis |
| post-obstructive diuresis may be multifactorial, resulting from... | excretion of excess salt and water retained during the obstruction, from a urea diuresis as the azotemia resolves, renal salt wasting caused by tubular injury, or from nephrogenic diabetes insipidus caused by the obstruction. |
| Intrinsic kidney injury may be divided into several broad categories of disease based on... | pathologic compartment involved or the pathophysiology of the renal disease |
| What are the (5) categories of intrinsic acute kidney injury? | • Acute tubular necrosis (ATN) • Acute interstitial nephritis (AIN) • Acute glomerulonephritis (AGN) • Acute vascular syndromes • Intratubular obstruction |
| ____ is the most common form of intrinsic acute kidney injury, accounting for approximately 85% of cases of intrinsic acute kidney injury. | Acute tubular necrosis |
| What are the major causes of ATN? | ischemia, nephrotoxic exposure, and sepsis |
| What things can lead to ischemic ATN? | prolonged prerenal azotemia, hypotension, hypovolemic shock, cardiopulmonary arrest, cardiopulmonary bypass, sepsis |
| What things can lead to nephrogenic ATN? | Exogenous toxins (drug induced):radiocontrast agents, aminoglycoside antibiotics, amphotericin B, cisplatinum, acetaminophen. Endogenous toxins (pigment nephropathy): hemoglobin, myoglobin |
| ATN pathophysiology | cell necrosis patchy; loss of normal morphology of tubular epithelial cells; loss of normal apical brush border + cell polarity->disrupted tubular transport->damaged cells sloughed into lumen (cell casts); intense renal vasoconstriction+endothelial injury |
| loss of GFR in ATN has been attributed to three processes: | • Renal vasoconstriction • Tubular obstruction from sloughed debris • Backleak of glomerular ultrafiltrate across the denuded tubular basement membrane |
| Describe the recovery of renal function in ATN | Remaining viable epithelial cells dedifferentiate, proliferate and spread across the denuded basement membrane, followed by re-differentiation and re-establishment of cell polarity. |
| What are the different (4) phases of ischemic ATN? | Initiation (acute ischemia), extension (endothelial injury, vasoconstriction, inflammation lead to ATN), maintenance (inflammation, endothelium cured, tubular repair), recovery (of tissue and GFR) |
| Describe the clinical presentation of patients with ATN: history | acute illness, medication history, exposure to other nephrotoxins, episodes of hypotension |
| Describe the clinical presentation of patients with ATN: physical examination | assessment of hemodynamic states, volume status + features of associated illness |
| Describe the clinical presentation of patients with ATN: laboratory data | a.BUN:Creatinine < 10:1 b.oliguric/non-oliguric c.Isosthenuric urine (osmolality ~ 300 mmol/L, SG ~ 1.010) d.Evidence of renal sodium wasting (urine sodium > 40 mmol/L, FENa > 0.02) e.Urine sediment |
| What urine sediment would you see in intrinsic AKI? | tubular epithelial cells and epithelial cell castsgranular casts (“muddy” brown casts |
| Treatment of ATN | essentially supportive; no pharmacological therapy shown effective at preventing or treating establish ATN; acute dialysis or hemofiltration may be necessary to support patients with severe renal injury or overt organ failure |
| ATN prognosis | depends on severity of renal failure + comorbidities: non-oliguric: better prognosis than oliguric due to less degree of cellular injury; overall mortality associated with ATN is ~50%; survivors: 90% see recovery of renal function within 2-4 wks |
| Acute interstitial nephritis (aka allergic interstitial nephritis): definition | immune mediated form of acute kidney injury characterized by lymphocytic infiltration of the interstitium |
| AIN accounts for ~ ___% of cases of intrinsic acute kidney injury | 5-10 |
| The “classic” presentation of AIN is the development of ___ | acute kidney injury accompanied by a triad of fever, rash and eosinophilia, however only 30% of patients actually present with this triad. |
| AIN Pathophysiology | The histologic findings in acute interstitial nephritis are the presence of a lymphocytic infiltrate in the kidney, frequently accompanied by eosinophils |
| Acute interstitial nephritis: most common etiologies | is most commonly drug-induced, but may be associated with a wide range of infections, systemic diseases and malignancy. |
| What drugs may result in AIN? | -penicillins -cephalosporins -sulfonamides -rifampin -phenytoin -furosemide -proton pump inhibitors -NSAIDs (may have atypical presentation with nephrotic range proteinuria and absence of eosinophilia) |
| What are the most common infective etiologies of AIN? | • bacterial • viral • rickettsial • tuberculosis |
| What are the most common systemic etiologies of AIN? | -systemic lupus erythematosus -sarcoidosis -Sjögren’s syndrome -tubulointerstitial nephritis and uveitis (TIN) |
| What is the typical clinical presentation of patients with AIN (History, physical exam, lab findings, urine findings) | preceding illness or drug exposure; fever/rash; eosinophilia; non-nephrotic proteinuria, hematuria, pyuria, WBC casts, eosinophiluira (nonspecific, but NPV>90%) |
| What is the treatment for AIN? | Remove underlying trigger (remove offending drug, treat underlying infection, or treat underlying systemic disease); glucorticoid treatment uncretain, but may be used in patients that fail to respond to more conservative therapy |
| These patients present with a nephritic urine sediment with hematuria and RBC casts. An exact diagnosis usually requires a kidney biopsy. | Acute glomerulonephritis |
| What are the possible etiologies for acute glomerulonephritis (GN)? | •poststreptococcal GN •postinfectious GN •endocarditis-associated GN •systemic vasculitis •thrombotic microangiopathy (hemolytic-uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP)) •rapidly progressive GN (RPGN) |
| Atheroembolic disease: pathophysiology | aka cholesterol embolization: due to rupture of atheromatous plaques in aorta with embolus into distal arterioles |
| What are the findings in patients with Intrinsic Kidney Injury secondary to atheroembolic disease? | livedo reticularis, microinfarcts of digits (blue toe syndrome); initial shower of emboli usually does not result in vascular occlusions (but triggers secondary inflammatory response that results in fibrosis)-->subacute kidney progression |
| In atheroembolic disease, the pathognomonic finding is of ____ | biconcave, needle-shaped clefts on histologic examination of blood vessels. These cholesterol clefts result from the dissolution of the cholesterol crystals in the emboli during tissue fixation. |
| ____ _____ also represents a relatively uncommon form of acute kidney injury that does not readily fit into the traditional ATN/AIN/AGN classification scheme | Intratubular obstruction |
| intratubular obstruction may result from either ... | crystaline material such as uric acid in the tumor lysis syndrome, calcium oxalate following ethylene glycol ingestion or drug crystals (e.g., acyclovir), or proteinaceous material, as seen in light chain cast nephropathy seen in multiple myeloma |
| BUN:Cr >20:1, UNa < 20, FENa <0.01, urine sediment normal | Prerenal AKI |
| BUN:Cr >20:1, UNa > 20, FENa variable, urine sediment normal or RBCs | Postrenal AKI |
| BUN:Cr <10:1, UNa > 40, FENa >0.02, urine sediment has muddy brown casts, tubular epithelial cells | Intrinsic ATN |
| BUN:Cr <20:1, UNa > 20, FENa >0.01, urine sediment shows WBCs, WBC casts, RBCs, eosinophils | AIN AKI |
| BUN:Cr variable, UNa < 40, FENa <0.01, urine sediment shows normal or RBCs, eosinophils in atheroembolic disease | Vascular AKI |
| BUN:Cr variable, UNa variable, FENa variable, urine sediment shows crystal or presence of immunoglobulin light chanins (Bence Jones Proteins) in urine | Intrabubular Obstruction |
| How should prerenal azotemia be managed? | 1Volume repletion 2Discontinue diuretics 3Discontinue other offending drugs (NSAIDs, ACEI, ARBs) 4Inotropic support for cardiac dysfunction |
| How should obstructive nephropathy be managed? | Bladder catheterization for lower tract obstruction, Percutaneous nephrostomies or ureteral stents for upper tract obstruction |
| How should intrinsic acute kidney injury be treated? | Majority of etiologies have no specific treatment-->focus on general supportive management (fluid management, bicarb supplement, K+ restriction, Phosphate restriction, change drug dose to avoid drug toxicity, nutrition support; renal replacement surgery |
| What are the indications for renal replacement therapy in acute kidney injury? | Volume overload unresponsive to diuretics; Metabolic acidosis unresponsive to alkali replacement; Persistent hyperkalemia Overt uremic symptoms such as pericarditis and encephalopathy; Severe azotemia (BUN > 80-100 mg/dL) in the absence of uremic symptom |
Created by:
karkis77
Popular Physiology sets