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Renal 1
Clinical Medicine: Renal Part 1
| Term | Definition |
|---|---|
| Where are most electrolytes and water reclaimed? | Proximal convoluted tubule |
| What happens to BUN and Creatinine when you are dehydrated? | Osmotically active urea is reabsorbed, so BUN goes way up. Creatinine is also reabsorbed, but not as fast of a rate. BUN/Creatinine ratio is disproportionately raised. |
| In an inflammatory process, what might a U/A be positive for? | Dysmorphic RBCs, RBC casts, protein. |
| What is an example of a non-inflammatory process and what would the U/A be positive for? | Diabetes: basement membrane destruction. U/A (+) for protein, not blood. |
| What is a measure of functional capacity of the kidney? What is normal? | Glomerular Filtration Rate (GFR); 120 mL/min |
| What does dapagliflozin do? Adverse? | reduces reabsorption of glucose and is utilized for treatment of type II diabetes mellitus. Adverse: Increases UTIs |
| What is the renal threshold for glucose? What happens when it is reached? | 180 mg/dL; anything else spills into the urine. |
| Where is the action of loop diuretics? Thiazide diuretics? Greatest effect on loss of sodium? | Loop: Loop of Henle (imagine that!); Thiazide: Distal Tubule; Loop has greatest effect on loss of sodium. |
| Function in proximal tubule? (3) | 1) Na+, other ions, amino acids, glucose and other substances are reabsorbed. 2) Water follows passively. 3) Filtrate volume reduced by 60-70% |
| Function in descending limb of Loop of Henle (2) | passive by diffusion gradient; 1) water exits passively and to a lesser extent: solute enters group. 2) Filtrate volume reduced by 15% |
| Function in the ascending limb of Loop of Henle (2) | 1) Na+, Cl-, K+ transported out of filtrate (pumped out) 2) Water remains |
| Function in distal tubules and collecting ducts | 1) Water movement regulated by ADH. 2) Sodium, chloride, potassium, hydrogen ion movement regulated by aldosterone |
| What is the sensor for the tubuloglomerular feedback response? | macula densa |
| What contains renin and what causes it to be released? | Juxtaglomerular apparatus; hypotension (w/reduced BP) leads to stimulation of the SNS and increased release of renin. |
| Countercurrent multiplication | produces hypertonic medullary interstitum using 1) loop of Henle and 2) Vasa recta (capillaries around loop). Maintains hypertonic environment in inner medulla, reabsorbs NaCl w/o water dilutes tubular fluid. |
| How does a hyperosmotic gradient affect concentration and volume of urine? | Establishes environment for regulation |
| Principal (P) cells: | primarily secrete K and participate in aldosterone-stimulated Na reabsorption. Found in collecting tubule. |
| Intercalated (I) cells: | responsible for acid-base regulation. P cells reabsorb Na, so either Cl is also reabsorbed or K secreted in exchange. Also found in the collecting tubule. |
| What hormones affects the collecting tubule? What would happen w/o the hormones? | ADH and aldosterone. Without them, fluid would simply flow through the tube to the bladder. |
| 2 urine concentrating mechanisms when large volume of water consumed | 1) must eliminate w/o wasting large amounts of electrolytes 2) kidneys produce large volume of dilute urine |
| 2 urine concentrating mechanisms when drinking water is unavailable | 1) kidneys produce small volume of concentrated urine 2) removes waste and prevents rapid dehydration |
| AntiDiuretic Hormone: where does it come from? How does it work? Too much? | High NA in blood stimulates posterior pituitary to secrete ADH. ADH opens water channels on collecting ducts leading to increased water reabsorption (dilutes Na concentration). TOO MUCH ADH can come from small lung Ca. |
| Aldosterone: how does it work? Aldosterone inhibitors? | causes reabsorption of water and Na (K secretion). Inhibitors: spironolactone causes Na loss and potential side effect is hyperkalemia or hyponatremia |
| T/F: Decreased BP -> ^ renin from juxtaglomerular cells -> A1 -> A2 -> ^ systemic vascular resistance (SVR) -> ^ arterial pressure -> ^ blood volume and cardiac output | True! Memorize and understand this process! |
| Atrial Naturetic Peptid (ANP) | for fluid overload; released by atrium in response to atrial stretching due to increased blood volume. Inhibits Na and water reabsorption and ADH secretion, promoting secretion of Na and water. |
| Renin | produced by JGA (juxtaglomerular apparatus) causing production of angiotensin II stimulating aldosterone and thirst, so is a potent vasopressor. Saves water, increases BP |
| 3 hormones produced by kidney | Renin, EPO (erythropoietin) (primary cause of anemia w/ chronic renal failure [normochromic/cytic], secondary w/iron deficiency anemia), Vitamin D3 (involved in calcium homeostasis (would effect high PTH) |
| T/F: Dipstick can detect immunoglobulins | False, therefore multiple myeloma cannot be detected |
| T/F: urinary protein will miss microalbumin | True |
| What test did the quantitative spot urine test replace? | 24 hour urine test |
| Eosinophils in blood and urine are highly suggestive of: | AIN (acute interstitial nephritis) (sulfa drug reactions and others) |
| What disease processes might you see cellular casts in? White casts? Red casts? Granular casts? Waxy casts? | Ischemia, infarction, nephrotoxicity (indicates acute tubular injury). White: leukocytes incorporated into casts during tubulo-interstitial inflammation. Red: glomerular injury. Granular: form as a stage in degernation of cellular casts. Waxy: chronic DZ |
| Creatinine | comes from a breakdown of creatine phosphate in muscle; blood levels rise with reduce kidney filtering; there is a lag time |
| T/F: Rising BUN/Creatinine ratio indicates over-diuresis and reduced renal perfusion | True |
| What are the variables for GFR estimation? (3) | Age, ideal body weight, blood creatinine. |
| T/F: measurement of CrCl by using a time urine collection provides a more accurate estimate of GFR than prediction equations do | False, equations are very accurate! |
| Imaging of choice for renal cysts and renal parenchyma? | Ultrasound! |
| Imaging choice for renal masses, infections, calculi? | CT |
| Azotemia | increased BUN/Creatinine, discovered incidentally, caused by almost any type of underlying renal disease |
| Uremia and Sx | accumulation of waste products in blood, caused by almost any type of underlying renal disease, Sx: HTN, anemia, edema, oliguria |
| T/F: Chronic Kidney Injury can occur with or without a decreased GFR | True, Reduction in GFR not necessary. |
| T/F: Chronic Kidney Disease is decreased kidney function or kidney damage for 6 or more months | False, 3 |
| Most common cause of renal failure in America | Diabetes |
| GFR stages (don't know if we have to know them but here they are) | Stage 0: At risk patients Stage 1: Kidney damage w/ normal GFR Stage 2: GFR 60-89 Stage 3: GFR 30-59 Stage 4: GFR 15-29 Stage 5: GFR <15 or dialysis |
| Stage 0: at risk patients: (8) just know a few | DM2, HTN, chronic NSAID use, minority, Age>60, SLE, transplanted kidney, family hx of kidney disease |
| AKI staging | A) pre-renal (inadequate renal perfusion) B) Intrinsic renal (direct toxic effect on kidneys or prolonged renal C) Post-renal (any form of obstruction) |
| Pre-Renal | Hemodynamic: HypoTN (shock), hypovolemia (hemorrhage, volume depletion through diarrhea etc), renal hypoperfusion (ACEI/ARBs, NSAIDS), Edema states (CHF, hepatic cirrhosis, nephrotic syndrome) |
| Inflammatory process of damage to glomerulus | Nephiritc |
| Non-inflammatory process of damage to glomerulus | Nephrotic |
| Where are most smaller proteins usually almost completely reabsorbed? | Proximal convoluted tubule (PCT) |
| Normal protein excrection? Normal albumin excretion? | <150mg; <30mg |
| Dual significance of proteinuria? | 1) associated with progressive kidney disease. 2) associated with increased cardiovascular risk |
| T/F: Renal disease is both a cause and a consequence of hypotension.` | I know, I got ya. False, cause and a a consequence of HYPERtension. Don't rush through questions. |
| 3 pathophys causes of proteinuria | 1) Overload (over production of filterable proteins as seen in multiple myeloma, rhabdo etc.) 2) Glomerular (increased permeability acrosss damaged basement membrane. 3) Tubular: (faulty reabsorption of filtered proteins seen in interstitial nephritis |
| What levels of albumin can a normal dipstick detect? Ultrasensitive dipstick? | <300mg/day; 30-300 mg/day |
| What is mesangium? | connective tissue holding everything together |
| 3 progressions of nephritic spectrum and 2 of nephrotic spectrum | Nephritic: 1) asymptomatic glomerular hematuria 2) nephritic syndrome 3) glomerulonephritis; Nephrotic: 1) Asymptomatic proteinuria 2) nephrotic syndrome. |
| Nephritic spectrum (3) | 1) dysmorphic RBCs 2) Red cell casts 3) 0.3-3 grams of protein |
| 4 Sx of Nephritic syndrome | 1) HTN 2) Edema (periorbital, scrotal) 3) Hematuria 4) findings of systemic disease (ex: SLE) |
| Difference between focal nephritic and diffuse nephritic. Nephrotic? | focal has red cells, occasionally red casts, and mild proteinuria; where diffuse has a heavier proteinuria and has a "full house" of urinary sediment. Nephrotic has heavy proteinuria and lipiduria but few cells or casts. "Bland urine" |
| RBCs, casts, moderate proteinuria with low complement and history of group A beta hemolytic strep. Sudden onset. Elevated anti-streptolysin antibody. Bx needed? Tx? | Postinfectious Glomerulonephritis. Bx usually not necessary. Treat underlying strep, supportive Tx |
| RBCs, casts, moderate proteinuria with low complement. Renal Bx directs therapy, doesn't Dx. 4x more in younger women | Systemic Lupus Erythematous: autoantibody disorder causing |
| 4+/6 required for Dx of SLE | 1) Malar rash 2) Discoid rash 3) photosensitivity 4) Oral/nasal ulcers 5) arthritis 6) serositis (pleuritis or pericarditis) |
| RBCs, casts, moderate proteinuria with low complement, young patient requiring Bx for Dx. Pt has hepatitis C (could have something else as well like SLE). Often idiopathic. | Membranoproliferative glomerulonephritis. MPGN |
| RBCs, casts, moderate proteinuria with low complement. Cold-precipitable immunoglobulins usually due to hepatitis C. Mild increase of ALT, AST on LFT. Causes purpura/necrotizing skin lesions, arthralgias, fever, hepatosplenomegaly. | Cryoglobulin Associated Glomerulonephritis. Interferon-alpha may be of benefit. |
| RBCs, casts, moderate proteinuria with low complement. Rare disease usually because patient is already Tx w/underlying condition. Occurs 10-14 days after acute infection due to development of immune complex-mediated injury. | Systemic Bacterial Endocarditis (SBE)-associated glomerulonephritis. |
| RBCs, casts, moderate proteinuria with normal complement, ANCA negative with a certain deposition in glomerular mesangium. Inherited susceptibility with unclear inciting cause. MOST COMMON primary glomerular disease worldwide. Occurs w/ onset of virus. | IgA Nephropathy. Can lead to transient renal failure. ACEI/ARB are Tx...lower protein. Treat only if disease is progressive. |
| RPGN | Rapidly Progressive Glomerular Nephritis. |
| T/F: There are no specific serological tests for Dx IgA | True. Bx required. |
| RBCs, casts, moderate proteinuria with normal complement, ANCA negative more common in children w/ tetrad of Sx: 1) abd pain 2) renal disease 3) palpable purpura 4) arthritis (more common in adults). IgA deposits due to immune complex rxn | Henoch Schonlein; Doesn't require renal Bx for Dx, but skin Bx can help. Will present similarly to IgA disease. Tx: usually self-limiting but steroids can help. Immunosuppressives not very beneficial. |
| RBCs, casts, moderate proteinuria with normal complement, ANCA negative with pulmonary hemorrhage in older patients. Hemoptysis after URI, nephritic urinary sediment, | Goodpasture's/Anti-Glomerular Basement Membrane; Tx: high dose IV steroids followed by oral prednisone. Plasma exchange every other day until anti-GBM antibody titire is negative. |
| RBCs, casts, moderate proteinuria with normal complement, ANCA positive with fever, rhinorrhea, nasal ulcers, sinus pain, polyarthralgias, cough, hemoptysis, SOB, CXR: nodular lesions | Granulomatosis w/polyangiitis (Wegner's) |
| ANCA | Anti-Neutrophil Cytoplasmic Antibody; Associated w/small vessel vasculitides; are antibodies directed against certain proteins in cytoplasmic granules of neutrophils and monocytes. |
| Treatment for Pauci-immune glomerulonephritis (ANCA positives) | Initiate early, high dose corticosteroids, cytotoxic agents. |
| Characteristics of Nephrotic Spectrum: (3) | 1) Bland urine sediment including >3 grams/day of protein, hypoalbuminemia, peripheral edema, hyperlipidemia. 2) Frothy urine due to excessive protein. 3) Xanthelasma |
| No casts, few RBCs, heavy proteinuria where albuminiuria precedes a decline in GFR, retinopathy coincides with nephropathy. | Diabetic nephropathy. (usually have DM for 10+ years). Intervene before deterioration (so screen for protein in urine). Bx Dx, but rarely needed |
| No casts, few RBCs, heavy proteinuria, can be outcome of Multiple Myeloma, plasma cell dyscrasias. Extracellular deposition of fibrous protein amyloid in one or more sites of body | Amyloidosis |
| No casts, few RBCs, heavy proteinuria, associated with coagulopathy. Antigen on podocytes. Spike and dome pattern on renal Bx, eval for possible underlying malignancy. Most common cause of primary nephrotic syndrome in adults. | Membranous Nephropathy |
| No casts, few RBCs, heavy proteinuria, idiopathic/autoimmune, could be secondary from toxins, genetics, infections (esp HIV), obesity, familial, heroin nephropathy | Focal Segmental Glomerulosclerosis (FSGS) |
| No casts, few RBCs, heavy proteinuria often precipitated by bee sting, viral infection and is associated w/ Hodgkin's lymphoma. Dramatic weight gain, pitting edema. | Minimal Change Disease; If Bx performed, electron microscopy will show fusion of podocytes. Tx: Oral corticosteroids (prednisone 60mg/day empirically) |
| No casts, few RBCs, heavy proteinuria, rapid decline GFR, presents similarly to focal segmental glomerulosclerosis | HIV Nephropathy. Tx: anti-retroviral Tx may slow progression |
| 5 complications from nephrotic syndrome | 1) severe protein malnutrition 2) hypercoagulability 3) acute renal failure 4) infx 5) iron, copper, zinc, vitamin D deficiency |
| Nephrotic syndrome Txs (3) | 1) underlying condition 2) ACEI/ARB 3) Salt restriction |
| 6 risk factors for acute kidney injury | 1) age 2) race 3) genetics 4) HTN 5) DM 6) metabolic syndrome |
| RIFLE Criteria | Risk, Injury, Failure, stage 4 Loss, ESRD (stage 5) |
| Predictors of mortality | multisystem failure, mechanical ventilation, hypoalbuminemia, hyperbilirubinemia, severe lactic acidosis; all require dialysis |
| 5 clinical findings in acute kidney injury | 1) volume overload 2) hyperkalemia 3) uremia 4) metabolic acidosis 5) lab findings (elevated BUN/Creatinine, anemia) |
| T/F: BUN most widely used parameter for assessment of GFR | False, serum creatinine |
| T/F: Serum creatinine lags behind both renal injury and recovery | True |
| Acute elevvation of BUN w/o actual renal injury (6) | 1) protein loading 2) catabolic state with severe sepsis 3) GI bleeding 4) corticosteroid therapy 5) tetracycline 6) intravascular volume depletion |
| T/F: increase in BUN or creatinine implies at least 75% of nephrons are not functioning | True |
| 4 things you can't do with elevated BUN or creatinine | 1) differentiate pre, intrinsic, post renal processes 2) differentiate btwn acute/chronic 3) differentiate reversible/irreversible processes 4) differentiate progressive vs non-progressive |
| What is the most common cause of acute kidney injury? | pre-renal, due to hypoperfusion |
| Autoregulation | kidneys maintain GFR and RBF relatively constant in systolic BP range of 80-160 |
| ACEI/ARBs | prevent efferent renal ateriolar constriction (outward arteriole remains dilated) |
| NSAIDs/Prostaglandins | prevent afferent afferent arteriolar vasodilation (in coming arteriole stays constricted) |
| Decreased perfusion pressure on afferent/efferent arterioles | Dilation of afferent and constriction of efferent |
| NSAIDs on afferent/efferent arterioles | constriction of both afferent and efferent |
| ACEI/ARB on afferent/efferent arterioles | dilation of afferent and efferent (esp efferent) |
| Abdominal compartment syndrome: what is it, what certain pressures do, Dx | decreased renal perfusion associated w/ ^ intra-abd pressure. Oliguria when pressure is 15mmHg+, anuria when pressure is 30mmHg+. Lower renal flow increases water retention, which is unnecessary b/c body not losing fluid. Dx: Intravesicular manometry |
| Abdominal compartment syndrome: Tx and Prognosis | abdominal decompression; paracentesis if massive ascites, surgical decompression required in majority of patients. Renal failure usually recovers quickly after surgery. |
| Hepatorenal Syndrome (HRS): Pathology and defining feature | occurs at end stages of liver disease; resulting from profound renal vasoconstriction. Highly resembles pre-renal azotemia, but a defining feature is lack of improvement w/volume expansion. |
| Examples of nephrotoxic endogenous and exogenous causes | Endo: Rhabdo (heme pigments [myoglobin/hemoglobin]); Exo: IV contrast |
| Predisposing factors to contrast-induced acute kidney failure (8) | 1) old age 2) pre-existing kidney disease 3) volume depletion 4) diabetic nephropathy 5) CHF 6) MM 7) repeated doses of contrast 8) NSAIDs/ACEI/ARB |
| Pathogenesis of contrast-induced AKI | hemodynamic alterations and tubuloglomerular feedback leading to renal ischemia. rapid vasodilation -> prolonged vasoconstriction -> reduction of total renal blood flow. Dialysis rarely needed. |
| Prophylactic strategies for contrast-induced AKI | 1) use contrast only when necessary 2) good hydration 3) minimize contrast volume 4) non-ionic contrast media |
| Rhabdomyolysis: What it is, Dx, Dx | common after crush injuries, seizures, burns etc; Dx w/ serum creatinine where dipstick will be positive for blood but there won't be RBCs on microscopy. Tx: supportive |
| Acute Tubular Necrosis: Dx, Tx, Sediment, Prognosis | Dx: Hx, Tx: supportive, Sediment: granular casts, muddy-brown casts, renal tubular epithelial cells; 80% recover if initial insult reversed. |
| 2 key features in allergic interstitial nephritis U/A | 1) Sterile pyuria: white cells that won't grow, Cx keeps coming back negative. 2) Eosinophiluria |
| DD for eosinophiluria (4) | Prostatitis, RPGN, Bladder Cancer, Renal atheroembolic disease |
| Renal Atheroembolic Disease | part of a multisystem that can affect kidneys due to cholesterol embolization. |
| Post-renal causes of AKI: 2 major classifications | Intra-renal obstruction (drugs, acute uric acid nephropathy) and Extra-renal obstruction (bladder [BPH], urethra [stricture], renal pelvis/ureter [stone, clot, tumor etc) |
| Dx and labs with AKI | CBC, serology, U/A, urinary sediment, U/S of kidneys, serum creatinine increase (with BUN usually following Scr increase) |
| Fractionated excretion of sodium | low Na excretion w/pre-renal; high Na excretion w/ intrinsic renal |
| FENa <1% | pre-renal state |
| FENa>1% | intrinsic state (ATN) |
| Urine Na (UNa) above 40? | ATN (intrinsic state) |
| Urine Na (UNa) below 20? | pre-renal |
| Urine osmolaltiy below 350? | ATN (intrinsic state) |
| Urine osmolality above 500? | pre-renal |
| Hydronephrosis | Post-obstructive renal failure. |
| Hemoglobin concentration in acute and chronic renal failure | Normal in acute, low/anemia in chronic |
| Renal size in acute and chronic renal failure | Normal in acute, reduced in chronic |
| Renal osteodystrophy in acute and chronic renal failure | Absent in acute, present in chronic |
| Peripheral neuropathy in acute and chronic renal failure | Absent in acute, present in chronic |
| Serum creatinine concentration | Acute reversible increase, chronic irreversible |
| Chronic Kidney Disease: Reversible? Can you stop the progression? How can you do this? Risk factor for other diseases? | Rarely reversible, can stop or slow progression. Control BP, glucose, lipids, stop NSAIDs. CV Disease |
| 2 broad sets of mechanisms of damage in CKD | 1) Initiating/original: genetic, HTN, immune complex deposition and inflammation, toxin exposure. 2) progressive mechanisms involving hyperfiltration and hypertrophy of remaining viable nephrons |
| Kidney failure (category 5 CKD) definition | GFR<15 or dialysis/transplantation |
| ESRD (end stage renal disease) | patient treated w/dialysis or transplantation |
| T/F: Abnormal urine sediment indicates renal damage regardless of GFR | True, same with proteinuria |
| Main cause of death in CKD? | microinfarctions |
| Causes of CKD | Diabetic glomerular disease (most common in US), glomerulonephritis, hypertensive nephropathy, autonomic dominant polycystic kidney disease. Diabetes primary Dx for those starting dialysis |
| Kidney damage causing HTN leading to irritation of kidneys | Nephrosclerosis |
| Hyaline arteriolarsclerosis | small arteries and arterioles thickenedand scarred eventually leading to insufficiency and failure |
| Renal artery stenosis: causes, labs, imaging | 90% atherosclerosis, 10% fibromuscular dysplasia; Lab: elevated renin level; Imaging: renal artery U/S |
| Management/Tx for Atherosclerosis (6) | ACEI/ARB and diuretic possibly, monitoring of creatinine and BP, LDL to goal, DM management, smoking cessation, anti-platelets |
| What is vesicoreteral reflux? | flow back into kidney |
| Tubulointerstitial disease causes (7) | 1) drug hypersensitivity 2) heavy metals 3) sarcoidosis 4) analgesic nephropathy 5) vesicoreteral reflux 6) sickle cell nephropathy 7) idiopathic |
| Tubulointerstitial disease: characteristics (6) | 1) Kidney size small and contracted 2) decreased urinary concentrating ability 3) hyperchloremic metabolic acidosis 4) reduced GFR 5) proteinuria less than 2 grams 6) Hyperkalemia |
| Pathophysiology of polycystic kidney disease | genetic! |
| Analgesic nephropathy: drugs of concern, pathology | NSAIDs, aspirin, phenacetin; pathology: tubulointerstitial inflammation, papillary necrosis. |
| What stages of CRF does uremia occur in? 3 pathophys manifestations? | Stages 3 and 4 1) accumulation of toxins 2) loss of other fns like electrolyte homeostasis and hormone regulation 3) progressive systemic inflammation |
| Uremic syndrome: What does it cause? Sx? | 1) anemia 2) malnutrition 3) alteration of plasma levels of many hormones. Constitutional Sx, pruritis, seizure if severe. |
| 5 complications of CKD | anemia, bone disease, HTN, CVD, metabolic |
| Anemia due to CKD...2 causes; Work up; Tx; goal of anemia Tx | 1) decreased EPO production 2) Iron deficiency; work up: CBC, the irons, retic, peripheral blood smear; Tx: correct Iron or EPO (with ESAs); Goal: Hgb 10-11 |
| Metabolic Bone Disease: Manifestations | 1) abnormalities in calcium, phosphorus, PTH, vitamin D 2) abnormalities in bone turnover, mineralization 3) Vascular or other soft tissue calcification. |
| Renal osteodystrophy | Osteitis fibrosis cystica (high turnover bone disease), calcifications, osteomalacia (lack of bone mineralizations), adynamic bone disease (due to overtreatment of hyperparathyroidism [PTH high, Ca low, Vit D low]) |
| What is a potent inhibitor of vascular calcification? | Fetuin. Low levels can cause vascular axis. |
| What do you restrict if PTH is high? | Phosphate (cut out protein). Measure vitamin D |
| 3 Cardiovascular complications of CKI | 1) Hypertension 2) Coronary Artery Disease 3) CHF |
| What is an electrolyte imbalance in ACEIs, renin inhibitors and NSAIDs? Sx? Tx? | Hyperkalemia; weakness, lethargy, cramps, paresthesias, dysrhythmias (tall T waves, wide QRS, long PR intervals); Tx: Calcium gluconate (0-5 minutes with fast effect on cardiac conduction) |
| JNC8 guidelines for CKD in diabetics | BP goal <140/90, use ACEI or ARB but not both, lower proteinuria, treat hyperlipidemia, control A1C |
| 2 independent variables that predict long-term decline in renal function | 1) HTN 2) Proteinuria |
| 7 frequent causes of acute decline in GFR | 1) volume depletion 2) IV contrast 3) select ABX 4) NSAIDs 5) ACEI/ARBs 6) cyclosporin 7) obstruction of urinary tract |
Created by:
crward88
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