Term
| Excretion Function of Kidneys |
|
Definition
| filtration - water & waste removal (including drugs); reabsorption - regulation of electrolytes; secretion |
|
|
Term
| Endocrine Functions of Kidneys |
|
Definition
| renin - regulation of BP; erythropoetin - regulation of RBC production; prostaglandins; kinin |
|
|
Term
| Metabolic Functions of Kidneys |
|
Definition
| Vitamin D activation - regulation of Ca levels; metabolism - endogenous compounds, CYP P450; gluconeogenesis |
|
|
Term
| Normal Glomerula Filtration Rate (GFR) |
|
Definition
|
|
Term
| Amount of Filtered Na that is reabsorbed throughout tubules |
|
Definition
| 65% in PCT, 25% in loop of Henle, 5% in early DCT and 5% in late DCT |
|
|
Term
| Water Tubular Reabsorption |
|
Definition
| osmotically reabsorbed (except in collecting duct); responds to ADH in late DCT and collecting duct |
|
|
Term
| Tubular Reabsorption of Amino Acids |
|
Definition
| reabsorbed via active transport |
|
|
Term
| Things Secreted into tubule |
|
Definition
| organic ions (creatinine, histamine); drugs & toxins (cimetidine, probenecid, trimethoprim); other electrolytes (K, H+) |
|
|
Term
| Normal Rate of Urine Production |
|
Definition
| produced at rate of 1 mL/min |
|
|
Term
|
Definition
| increases in response to decreased renal perfusion pressure; released from juxtaglomerular cells in afferent arterioles |
|
|
Term
|
Definition
| increased in response to renin; potent vasoconstrictor; stimulates catecholamine release |
|
|
Term
|
Definition
| increased in response to Angiotensin II; stimulates Na & H2O reabsorption; promotes myocardial fibrosis & vascular dysfunction (tissue remodeling) |
|
|
Term
|
Definition
| endogenous hormone responsible for production of RBCs; 90% is created in kidney |
|
|
Term
|
Definition
| some activation occurs in kidney; required for regulation of Ca & bone formation |
|
|
Term
|
Definition
| sudden & rapid deterioration of renal fcn leading to electrolyte imbalances & inability to excrete nitrogenous waste products (azotemia); common complication in hospitalized pts (ICUs); usually reversible; 20% are drug-induced |
|
|
Term
| General Risk Factors of Acute Kidney Injury |
|
Definition
| advanced age; acute infection; pre-existing respiratory or cardiovascular disease; chronic kidney disease; dehydration; nephrotoxic drug use |
|
|
Term
| Clinical Manifestations of AKI |
|
Definition
| often assymptomatic; hyperkalemia; diminishing urine volume; increased Cr over SHORT period of time; fatigue, malaise, abdominal pain --> dyspnea, rales, peripheral edema --> arrhythmias, metabolic acidosis, altered mental status |
|
|
Term
| Pathophysiology of Prerenal Dysfunction (aka Prerenal Azotemia) |
|
Definition
| kidney hypoperfusion & decreased glomerular pressure; Physiologic response: maintain glomerular pressure & GFR --> activates SNA, activates RAAS, vasoconstriction of efferent arterioles & vasodilation of afferent arterioles, release of ADH |
|
|
Term
| Specific Pathophysiologies of Prerenal Dysfunction |
|
Definition
| decreased intravascular volume (blood loss, dehydration, hypoalbunimia); decreased systemic vascular resistance (hypotension, sepsis, anaphylaxis); decreased cardiac output (arrhythmias, HF, pulmonary HPN, valvular diseases); intrarenal hemodynamic changes (bilateral renal artery stenosis, hepatorenal syndrome, emboli, hypercalcemia, drug-induced) |
|
|
Term
| Drug-induced Prerenal AKI due to ACEIs or ARBs |
|
Definition
| occurs most often in renin-dependent states; 2 drug classes selectively dilate efferent arterioles, acutely decreasing glomerular perfusion pressure; especially harmful in hypovolemic/hypoperfusion states where RAAS has been activated (dilates afferent arterioles, constricts efferent arterioles); these drugs PREVENT constriction of efferent arterioles after RAAS activation, causing vasodilation, lowering GFR |
|
|
Term
| Drug-induced Prerenal AKI due to NSAIDs |
|
Definition
| in states of hypoperfusion, COX levels are increased to maintain glomerular perfusion pressure (dilation of afferent arterioles); these drugs inhibit COX, preventing vasodilation; especially harmful in states of hypoperfusion |
|
|
Term
| Most common cause of Prerenal AKI |
|
Definition
|
|
Term
|
Definition
| elevated BUN & Cr; high BUN:Cr (> 20:1); low urine Na; FENA% < 1%; Urinalysis: yellow to dark yellow, SG elevated, Uosm is elevated, hyaline casts present |
|
|
Term
| Managment of Prerenal AKI |
|
Definition
| correct volume deficits (blood transfusion, IV fluids); removal of inciting agents; correction of electrolyte disturbances; monitoring or removal of drugs that may accumulate to cause toxicity; emergent dialysis if indicated |
|
|
Term
|
Definition
| damage within the kidney or nephron; categorized by what structure is damaged: glomerulus, renal tubule, interstitium, vasculature |
|
|
Term
| Mechanisms of Glomerular Damage in Glomerulonephritis |
|
Definition
| systemic Ag-Ab complexes become trapped in glomerular capillaries (deposition): post-infectious glomerulonephritis, lupus nephritis, cryoglobulinemia; antineutrophil cytoplasmic antibodies (ANCA) formed against neutrophils & monocytes & do not cause immune deposits: Wegener's granulomatosis; Auto-Abs formed against glomerular basement membrane or epithelial cells: Goodpasture's syndrome |
|
|
Term
| Results of Glomerular Damage |
|
Definition
| 1) reduction of glomerular surface area --> reduction in amount of ultrafiltrate; 2) increased permeability of glomerular capillaries --> increased loss of protein & blood |
|
|
Term
| Drug-induced Glomerulonephritis |
|
Definition
| usually nephrotic; caused by rifampin, lithium, GOLD, NSAIDs |
|
|
Term
| Factors that Progress Glomerulonephritis |
|
Definition
| systemic & intraglomerular HPN; high dietary protein; hyperlipidemia; coagulation; Ca & PO4 abnormalities |
|
|
Term
| Evaluation of Glomerulonephritis |
|
Definition
| UA with microanalysis; 24-hr urine collection (urine protein & creatinine); PE & Pt Hx; Test for Abs (ANCA, complement) |
|
|
Term
| Glomerulonephritis NephrOtic Syndrome |
|
Definition
| etiology: systemic dx, non-inflammatory; Signs: edema, weight gain, fatigue; Lab Findings: PROTEINURIA >3.5 g/day, hyperlipidemia, lipiduria, hypoproteinemia, hypercoagulable state |
|
|
Term
| Glomerulonephritis NephrItic Syndrome |
|
Definition
| Etiology: INFLAMMATORY; Signs: hematuria, HPN, edema, decline in renal fcn; Lab Findings: proteinuria, PUS IN URINE, CELLULAR & GRANULAR CASTS |
|
|
Term
| Management of Glomerulonephritis |
|
Definition
| Goal: Reduce proteinuria; General Approach: Immunosuppressives (controversial - corticosteroids, cytotoxic agents, cyclosporine or mycophenolate); Supportive Therapy: restriction of dietary protein, Na, cholesterol, management of HPN, edema, hyperlipidemia |
|
|
Term
|
Definition
| cell death (necrosis) in tubule epithelium caused by prolonged or severe reduction in renal blood flow; Major Causes: ischemia (precursors: dehydration, shock, sepsis), nephrotoxins (exogenous: drugs, radiocontrast dye, heavy metals; endogenous: uric acid, myoglobin, hemoglobin); MOST COMMON CAUSE OF intrinsic renal failure |
|
|
Term
| General Risk Factors for Drug-induced ATN (acute tubular necrosis) |
|
Definition
| CKD, older age, concomitant drug use with other nephrotoxic or volume-depleting drugs, volume depletion, increased doses of nephrotoxic drugs |
|
|
Term
| Aminoglycoside-induced ATN |
|
Definition
| accumulation of aminoglycoside within epithelial cells of proximal tubule; inhibits phospholipases |
|
|
Term
| Amphotericin B-induced ATN |
|
Definition
| renal arterial vasoconstriction; direct toxicity to epithelial cell in distal tubule, altering cell permeability; additional risk factors: male sex, daily dose > or = to 35 mg, weight > or = to 90 kg |
|
|
Term
| Radiocontrast media-induced ATN |
|
Definition
| vasoconstrictors are released secondary to contrast media delivery to kidney --> reducing intrarenal perfusion (hemodynamic), direct toxicity to proximal tubule cells, occurs within 24-72 hrs after administration; Additional risk factors: DM, higher volume of media; Usually reversible |
|
|
Term
| Lab Evaluation of Acute Tubular Necrosis (ATN) |
|
Definition
| UA: brown-dark color, brown casts, renal tubular epithelium cells may be present; Urine Electrolytes: high urine Na, FENA%, low Uosm; In proximal tubular injury: hypokalemia, hypophosphatemia, hypomagnesemia, metabolic acidosis; In Distal Tubule Injury: hyperkalemia, metabolic acidosis, polyuria |
|
|
Term
| General Management of ATN |
|
Definition
| remove inciting agent; correction of electrolyte imbalances; monitor or removal of drugs that may accumulate to cause toxicity; emergent dialysis if indicated; IV fluid replacement; treatment of underlying problem |
|
|
Term
| Prevention of Toxicity from Exogenous Nephrotoxins in ATN |
|
Definition
| for aminoglycosides: drug level monitoring, risk increases with length of treatment (keep it short!); for Amphoterocin B: risk increases with higher dose & length of treatment, lipid-based formulations may be less nephrotoxic |
|
|
Term
| Prevention of Radiocontrast Media-induced ATN |
|
Definition
| avoid gadolinium-based agents; proper hydration before & after administration (NS vs NaHCO3); use of antioxidants (N-acetylcysteine [Mucomyst 600 mg PO BID day before & day of admin], ascorbic acid [Vitamin C]) |
|
|
Term
|
Definition
| occurs when interstitial tissue & surrounding tubule becomes inflamed; form of intrinsic dysfunction; hypersensitivity response; often present with fever, rash, arthralgias |
|
|
Term
| Major Causes of Interstitial Nephritis |
|
Definition
| drug-induced (most common): penicillins, sulfonamides, rifampin, cipro, NSAIDs, valproic acid, PPIs; Infectious diseases (bacterial & viral); idiopathic |
|
|
Term
| Lab Eval of Interstitial Nephritis |
|
Definition
| peripheral blood smear shows eosinophils; UA: WBCs, casts, eosinophils |
|
|
Term
| Management of Interstitial Nephritis |
|
Definition
| usually reversible; supportive management; for drug-induced: d/c drug, avoid rechallenge of drug; Possible corticosteroid therapy: methylprednisolone, prednisone |
|
|
Term
|
Definition
| possible causes: occlusion of larger renal arteries by emboli (atherosclerotic, thrombus); microangiopathies: inflammation or occlusion of small vessels (diffuse renal vasculitis, polyarteritis, thrombotic); hemolytic uremic syndrome; accelerated HPN |
|
|
Term
|
Definition
| UA: RBCs, casts, Heme +, red color; Serum: increased LDH, schistocytes; Radiology: CT or MRI showing renal vein thrombosis |
|
|
Term
| Management of Vasculitides |
|
Definition
| Supportive Treatment of: hypoproteinemia, thromboembolism, hyperlipidemia (low-lipid diet), HPN (restrict salt intake), edema (restrict salt intake, support stockings, edema), proteinuria (restrict protein intake); Immunosuppression: high dose steroids, cyclophosphamide, cyclosporine, mycophenolate mofetil; Plasma exchange (plasmapheresis) |
|
|
Term
|
Definition
| obstruction after nephron/kidney preventing urine flow out of tubule; Etiology: nephrolithiasis, urethral obstruction, BPH, uncommon causes (blood clots, bilateral ureteral stones), drug-induced; Pt presents with nausea, vomiting, fever, flank pain; can progress to intrinsic renal injury back into tubule |
|
|
Term
| Drug-induced Postrenal Azotemia |
|
Definition
| caused by anticholinergics (urinary retention); nephrolithiasis caused by: sulfonamides, foscarnet, allopurinol, acyclovir, methotrexate, indinavir; MoA of Nephrolithiasis: supersaturation of drug in urine forms crystals; Risk Factors for Nephrolithiasis: poor hydration, higher doses, longer treatment; |
|
|
Term
| Evaluation of Postrenal Azotemia |
|
Definition
| UA: little or no proteinuria, resembes prerenal azotemia initially (high Uosm, low urine Na, BUN:Cr > 20:1), once intrinsic injury has occurred (increased UNa, FENA% increases, other indices resemble intrinsic dx); Ultrasound to confirm obstruction |
|
|
Term
| Management of Postrenal Azotemia |
|
Definition
| increase fluid intake if due to nephrolithiasis; catheterization or stenting to relieve obstruction (results in diuresis --> possible dehydration, hydrate with IV fluids); pain management |
|
|
Term
| Normal Range for UA specific gravity |
|
Definition
|
|
Term
|
Definition
| increased in glomerular injury |
|
|
Term
|
Definition
| normal range is about 10 - 15:1; increased in acute hypovolemia/hypoperfusion (prerenal azotemia) b/c BUN reabsorbs easily when GFR acutely slow & Cr is NOT reabsorbed easily |
|
|
Term
|
Definition
| Normal range is 10-20 mEq/L |
|
|
Term
|
Definition
| = [(UNa/SNa)/(UCr/SCr)]*100; normal range is 1-2%; >2% = renal tubule damage, decreased reabsorption of Na; <1% = prerenal dysfunction, increased Na reabsorption |
|
|
Term
|
Definition
| < or = to 35% = prerenal dysfunction; > 50% = intrinsic renal dysfunction |
|
|
Term
|
Definition
| correlates with specific gravity; Increases when ADH is released/hypovolemia; decreased when renal tubule is damaged & cannot respond to ADH |
|
|
Term
| Lab Assessment of Pre-renal hypovolemia/hypoperfusion AKI |
|
Definition
| no cells, + hyaline casts; no or low protein; UNa < 20; Uosm > 400; UOsm:SOsm > 1.5; FENA% < 1%; BUN:Cr >20:1 |
|
|
Term
| Lab Assessment of Intrinsic Acute Tubular Necrosis AKI |
|
Definition
| broad, brownish granular casts; no or low protein; UNa >30; UOsm <350; UOsm:SOsm < 1.3; FENA% >2%; BUN:Cr < 20:1 |
|
|
Term
| Lab Assessment of Intrinsic Interstitial Nephritis AKI |
|
Definition
| white blood cells, eosinophils, white cell casts visible |
|
|
Term
| Lab Assessment of Intrinsic Glomerulonephritis AKI |
|
Definition
| RBCs visible, protein increased >100 mg/dL |
|
|
Term
| Lab Assessment of Post-renal Azotemia Obstruction AKI |
|
Definition
| no cells or bloody, red urine; low protein |
|
|
Term
| Glomerular Filtration Rate (GFR) |
|
Definition
| best indicator of renal fcn; expressed as volume of plasma filtered per unit time; normal range: 90 - 140 mL/min; cannot directly measure |
|
|
Term
|
Definition
| rate of filtration + rate of secretion - rate of absorption |
|
|
Term
| Factors Affecting Serum Conc of Cr |
|
Definition
| gender (decreased in females); race (increased in blacks); diet (decreased in vegetarians, increased with higher meat consumption); muscular body habitus (increased); malnutrition, amputation, muscle wasting disease (decreased) |
|
|
Term
| Estimated Creatinine Clearance (Cockcroft-Gault Equation) |
|
Definition
| [(140-age)* weight (kg)]/[72 * SCr]; multiply by 0.85 for females; recommended only in stable renal fcn |
|
|
Term
| IBW (Ideal Body Weight) Equations |
|
Definition
| For males: = 50 kg +/- 2.3 for every inch above/below 60 inches; For females: = 45.5 kg +/- 2.3 for ever inch above/below 60"; Use ABW if ABW < IBW; Use IBW if ABW > IBW but < 120% of IBW |
|
|
Term
| Adjusted Body Weight for obese pts |
|
Definition
| if ABW > 120% IBW, then use this equation: = 0.4*(ABW-IBW) + IBW |
|
|
Term
| Modification of Diet in Renal Disease (MDRD) Study |
|
Definition
| based on age, gender, race, & Cr; used in pts with CKD risk factors & GFR < 60 mL/min/1.73 m^2; more accurate estimation of GFR than Cockcroft-Gault |
|
|
