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75 Cards in this Set
- Front
- Back
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What are three ways in which to evaluate renal failure?
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Estimate duration
UA Glomerular filtration rate (GFR) |
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retention of BUN and Creatinine =
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Azotemia
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What are the specific details of a urine analysis?
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Urine should be examined within 1 h of collection
UA = Dipstick + Microscopy Dipstick examination includes specific gravity, protein, Hgb, glucose, ketones, bilirubin, nitrites and leukocyte esterase Microscopy evaluates for formed elements such as crystals, cells, casts and infecting organisms |
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Hematuria with dysmorphic RBC, RBC casts and protein in the urine analysis.
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Glomerulonephritis
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Protein and lipids revealed in the urine analysis.
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NephrOtic Syndrome
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Pigmented granular casts, renal tubular epithelial cells in the urine analysis.
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Acute Tubular Necrosis
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WBC (neutrophils and eosinophils), WBC casts, RBC and some protein in the urine analysis.
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Interstitial Nephritis or Pyelonephritis
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Proteinuria =
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> 150-160mg/24h in an adult
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Significant Proteinuria =
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> 1g/24h
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NephrOtic-range Proteinuria =
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> 3.5g/24h
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What are the functional reasons for proteinuria?
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Benign, in response to acute illness, or exercise.
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What is the reason for overload proteinuria?
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Overproduction of circulating filterable plasma proteins such as Bence Jones proteins in multiple yeloma, myoglobin in rhabdomyolysis and Hgb in hemolysis.
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What is the reason for glomerular proteinuria?
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Increased permeability across glomerular basement membrane (GBM)
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What is the reason for tubular proteinuria?
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Faulty reabsorption in proximal tubules in e.g. acute tubular necrosis, toxic injury etc.
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What is the TX for proteinuria?
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ACE Inhibitors
↓ Efferent arteriolar resistance in comparison to Afferent arteriolar resistance leads to ↓ glomerular capillary pressure and ↓ urinary protein excretion ARBs are just as good in ↓proteinuria and ↓ progressive renal dz |
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Hematuria: =
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> 3 RBC/ high power field
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False + on dipstick in testing for hematuria 2/2?
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vitamin C, beets or rhubarb, bacteria or myoglobin
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What is the cause of hematuria?
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Extrarenal
Renal (10% of cases) Glomerular: Immunoglobulin A nephropathy, Thin GBM dz, Post-infectious glomerulonephritis , Membranoproliferative glomerulonephritis, Systemic Nephritic Syndrome) Non-glomerular: Cysts, calculi, interstitial nephritis, renal neoplasm |
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What can be seen on ultrasonography with renal failure?
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Thickness and echogenicity of cortex, medulla and pyramids and distended collecting system
Kidney < 9cm in length in adult = significant irreversible renal dz Difference in size by > 1.5cm between both kidneys = unilateral renal dz Hydronephrosis or obstruction Renal mass Polycystic Kidney dz - string of pearls Assist in localizing kidney for percutaneous invasive procedure |
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What can be seen with intravenous pyelogram with renal failure?
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Now replaced by U/S or Helical CT
Used to be standard to evaluate urinary tract, pelvicaliceal system and localize renal stone Contrast injection Contrast relatively contraindicated in pts at ↑risk of acute renal failure (DM, Creatinine > 2mg/dl, dehydration) |
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No contrast necessary if looking for hemorrhage or renal stones
With contrast easy to identify cysts, neoplasms, renal vessels and ureters |
Imaging CT Scanning in renal failure
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Distinguishes renal cortex from medulla
Visualizes adrenals Good to evaluate renal mass when contrast is contraindicated Superior in Dx of renal A. stenosis |
Imaging MRI in renal failure
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What are the indications for a renal biopsy?
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Unexplained acute renal failure or chronic kidney dz
Acute nephrItic syndrome Unexplained hematuria and proteinuria Previously identified and treated lesion to plan future Tx Systemic Dz with kidney dysfunction (e.g. Systemic Lupus Erythematosus and others) Suspected transplant rejection |
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After renal biopsy, what is expected?
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Hematuria is common
Pt should remain supine for 4-6 hrs Monitor Hct (risk of major bleeding persists up to 72 h post Bx) Hold anticoagulation for 5-7 days post Bx |
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Sudden ↓ in renal function leading to inability to maintain fluid and electrolyte balance and to excrete nitrogenous wastes (marked by increased creatinine)
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Acute Renal Failure
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What are the signs and symptoms of acute renal failure?
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Nonspecific
Nausea, vomiting, malaise and altered MS Pericardial effusion with friction rub cardiac tamponade Arrhythmias 2/2 ↑kalemia Rales on lung exam 2/2 hypervolemia Abdominal pain and ileus Platelet dysfunction Encephalopathic changes (asterixis, confusion, seizures) |
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What are the laboratory findings of acute renal failure?
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↑ BUN and creatinine
↑ Kalemia, ↑ Phosphatemia EKG with peaked T waves, PR prolongation and QRS widening QT prolongation 2/2 ↓ calcemia Anemia 2/2 ↓ erythropoietin production Platelet dysfunction 2/2 uremic toxins that cause intrinsic platelet abnormalities as well as impairment in platelet-vessel wall interaction |
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Most common cause of acute renal failure, 40-80% of cases
Cause: Renal hypoperfusion Can be reversed with restoration of renal blood flow No parenchymal damage If hypoperfusion persists leads to ischemia leads to intrinsic renal failure |
Prerenal Azotemia - Acute Renal Failure
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Mechanism
↓ intravascular volume ( hemorrhage, GI losses, dehydration, excessive diuresis, burns and trauma) Change in vascular resistance (sepsis, anaphylaxis, ACE-I, Renal A. stenosis) ↓ cardiac output (leads to ↓renal perfusion in e.g. cardiogenic shock, CHF, PE, arrhythmias, valvular dz) BUN:creatinine ratio = 20:1 (2/2 ↑ urea reabsorption) |
Prerenal Azotemia - Acute Renal Failure
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Patients with prerenal failure failure have low fractional excretion of?
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Na
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What is the Tx for prerenal azotemia - acute renal failure?
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Depends on cause
Maintain euvolemia Monitor serum K Avoid nephrotoxic drugs |
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Least common cause of acute renal failure, 5-10% of cases
Reversible Mechanism: Urinary flow from both kidneys or a single functioning kidney is obstructed Obstruction can be constant or intermittent, partial or complete Causes: Urethral obstruction, bladder dysfct or obstruction, obstruction of both ureters or renal pelvises, BPH, bladder, prostate or cervical cancer etc. |
Postrenal Azotemia - Acute Renal Failure
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Sx: Anuria or polyuria, Abd pain
Initial Labs: ↑ urine osmolality ↓ urine Na ↑ BUN: creatinine ratio ↓ FeNa Labs after several days: ↑ urine Na (kidneys are unable to concentrate urine) |
Postrenal Azotemia - Acute Renal Failure
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How do you DX/TX Postrenal Azotemia - Acute Renal Failure?
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U/S
Bladder catheterization (if hydronephrosis and bladder enlargement) Then monitor lytes and keep pt hydrated 2/2 postobstructive diuresis |
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Up to 50% of acute renal failure cases
Is considered after pre- and post renal causes are excluded Sites of injury Tubules Interstitium Vasculature Glomeruli |
Intrinsic Renal Failure - Acute Renal Failure
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What are the three types of intrinsic renal failure?
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Acute tubular necrosis
Interstitial nephritis Glomerulonephritis |
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85% of intrinsic acute renal failure cases
Causes Ischemia Inadequate renal blood flow 2/2 prolonged hypotension or hypoxemia in setting of dehydration, shock and sepsis Nephrotoxin exposure Exogenous (more common than endogenous) Endogenous |
Acute tubular necrosis - Intrinsic Renal Failure - Acute Renal Failure
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What are two things responsible for causing acute tubular necrosis?
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Exogenous and endogenous nephrotoxins.
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Exogenous Nephrotoxins
Example: Aminoglycosides Non oliguric renal failure after 5-10 days Predisposing factors: Underlying renal damage, dehydration, advanced age Monitor peak and trough to prevent Gentamycin is as toxic as Tobramycin Streptomycin is least nephrotoxic Amphotericin B is toxic after dose of 2-3 g Mechanism: Severe vasoconstriction leads to tubular damage |
Cause of acute tubular necrosis
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Exogenous Nephrotoxins
Example: Radiographic contrast media Mechanism: Direct renal tubular epithelial cell toxicity and renal medullary ischemia Predisposing factors: Advanced age, preexisting renal dz, dehydration, diabetic nephropathy, CHF, multiple myeloma, repeated contrast exposure, recent exposure to nephrotoxin e.g. NSAIDs or ACE-I Greatest risk: DM + renal dysfunction Occurs 24-48h post contrast administration |
Cause of acute tubular necrosis
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Prevention of renal damage by exogenous nephrotoxin (contrast):
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NS IV for 12 h prior and 12 h post contrast
Some studies support: N-acetylcysteine (600 mg po q12h x 2 prior and post contrast OR 1200mg IV prior to contrast) |
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Endogenous Nephrotoxin
Myoglobinuria 2/2 rhabdomyolysis: In crush injury, or muscle necrosis from prolonged unconsciousness, seizures, cocaine and ETOH abuse Myoglobin is freely filtered across the glomerulus and reabsorbed in renal tubules Mechanism: Distal tubular obstruction and intrarenal vasoconstriction Labs: Serum Creatine Kinase > 20,000 -50,000 IU/L Urine appears dark, ↑ Phosphatemia, ↑ Uricemia Tx: Hydration |
Cause of intrinsic renal failure
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Endogenous Nephrotoxin
Hemoglobinuria 2/2 massive intravascular hemolysis in setting of transfusion reaction or in hemolytic anemia Tx: Reversal of underlying condition and hydration Hyperuricemia 2/2 intratubular deposits of Uric Acid crystals in setting of Chemotherapy (rapid cell turnover) Bence Jones protein 2/2 direct tubular toxicity and obstruction in setting of Multiple Myeloma |
Cause of intrinsic renal failure
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What are the lab findings for acute tubular necrosis?
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‘Muddy brown’ casts
↑ Kalemia ↑ Phosphatemia |
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What is the TX for acute tubular necrosis?
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Avoid fluid overload and ↑ Kalemia
High dose Furosemide (20-160mg po qd) – no affect on mortality Dialysis |
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What is the outcome or expectations for acute tubular necrosis?
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Clinical course in 3 phases
Initial injury Maintenance (1-3 weeks- several months - cellular repair and removal of tubular debris) Oliguric Non oliguric (better outcome) Recovery ( GFR begins to rise, BUN and creatinine decrease) Mortality rate: 20-50% in medical illness, 70% in surgical setting Nephrology referral improves outcome in acute renal failure! |
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10-15% of intrinsic renal failure
Mechanism: Interstitial inflammatory response with edema and possible tubular cell damage |
Interstitial nephritis - intrinsic renal failure
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What are the causes of interstitial nephritis - intrinsic renal failure?
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Causes:
Drugs (70% of cases; penicillin, cephalosporins, sulfonamides, NSAIDs, rifampin, phenytoin and allopurinol, PPIs) Infectious dz (streptococcal infections, leptospirosis, crytomegalovirus, histoplasmosis, Rocky Mountain spotted fever) Immunologic d/o (Systemic lupus erythematosus, Sjogren syndrome, sarcoidosis, cryoglobulinemia; these cause more often glomerulonephritis ) |
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What are the symptoms of interstitial nephritis - intrinsic renal failure?
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Fever
Transient maculopapular rash Arthralgias Eosinophelia Urine: RBC, WBC, WBC casts, proteinuria (especially if caused by NSAIDS), eosinophils |
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What is the prognosis and expected outcome for interstitial nephritis?
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Good prognosis, rarely progresses to ESRD
Worse outcome in oliguric failure and advanced age Recovery over weeks to months Tx Short course of corticosteroids |
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5% of cases, so relatively uncommon
Causes: IgA nephropathy (Berger’s dz) Peri or post infectious glomerulonephritis Endocarditis Lupus nephritis Cryoglobinemic glomerulonephritis (associated with hepatitis C virus) Membranoproliferative glomerulonephritis Anti-GBM-associated acute glomerulonephritis (if associated with pulmonary hemorrhage = Goodpasture syndrome) Wegener granulomatosis = systemic necrotizing vasculitis of small vessels affecting upper airway, pulmonary and skin vessles |
Glomerulonephritis
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What are the signs and symptoms, lab findings and DDX for glomerulonephritis?
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Signs and Symptoms
HTN, edema (periorbital and scrotal) Laboratory Findings Urine: Moderate protein (< 3g/d), RBC, RBC casts, WBC Complement levels (C3, C4, CH50) ASO titer Anti-GBM antibody levels ANCAs Antinuclear antibody titers Cryoglobulins Hepatitis Serologies Blood Cx Also consider Renal U/S or renal Bx |
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What is the TX for glomerulonephritis?
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High dose corticosteroids
Cytotoxic agents such as cyclophosphamide Plasma exchange in Goodpasture dz until chemotherapy takes effect |
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Affects ~ 20 Mill Americans, or 1 in 9 adults
Rarely reversible, leads to progressive ↓ in renal fct ↓ renal mass leads to hypertrophy of remaining nephrons and hyperfiltration (supranormal GFR) leads to progressive glomerular sclerosis and interstitial fibrosis |
Chronic Kidney Disease
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Stage GFR
1 ≥ 90 2 60-89 3 30-59 4 15-29 5 < 15 |
Chronic Kidney Disease staging
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Glomerulopathies
Primary glomerular dz (e.g. IgA nephropathy) Secondary glomerular dz (e.g. Diabetic nephropathy) Tubulointerstitial nephritis (e.g. drug hypersensitivity) Hereditary dz (e.g. Polycystic kidney dz) Obstructive nephropathies (e.g. nephrolithiasis) Vascular Dz (e.g. HTN, renal artery stenosis) |
Cause of Chronic Kidney Disease
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What are some symptoms of chronic kidney disease?
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Develop slowly, nonspecific, until renal failure is far advanced
Fatigue, weakness, malaise Anorexia, N/V, metallic taste, hiccups Irritability, difficulty concentrating, insomnia, memory deficit Pruritis, yellow skin, easy bruisability ↓ libido, menstrual irregularities CP from pericarditis |
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What are some signs of chronic kidney disease?
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HTN, rales, cardiomegaly, edema, pericardial friction rub
Uremic frost Uremic fetor = fishy odor of the breath |
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What are the lab findings and the image findings with chronic kidney disease?
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Previously ↑ BUN and creatinine
Anemia Metabolic acidosis ↑ Phosphatemia ↓ Calcemia ↑ Kalemia Urine: Broad waxy casts Small bilateral echogenic kidneys on U/S |
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↑ Kalemia (once GFR < 10-20 ml/min)
↑ risk of ↑ Kalemia even at lower GFR in cellular destruction (hemolysis or trauma) Dietary K (citrus fruit, salt substitutes containing K) Drugs that ↓ K secretion (amiloride, triamterene, spironolacotone , NSAIDs, ACE-I) Tx: Dietary K restriction and Na polystyrene sulfonate (Kayexalate) |
Complication of chronic kidney disease
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Acid-Base Disorders
Damaged kidney is unable to excrete the 1 mEq/kg/d of acid generated by dietary protein metabolism leads to metabolic acidosis Limited production of ammonia NH3 and limits buffering of H+ in the urine Excess H+ are buffered by Ca Carbonate and Ca Phosphate stores in bone to keep blood pH between 7.33-7.37 |
Complication of chronic kidney disease
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↑ risk of mortality and morbidity of CV dz
Accounts for 45% of deaths of pts on dialysis 95% of pts with chronic kidney dz die of CV causes Mechanism is unclear |
Complication of chronic kidney disease
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HTN (Tx with Na and H2O restriction, weight loss, drugs)
Pericarditis (believed to be 2/2 retention of metabolic toxins; absolute indication for initiation of hemodialysis) CHF (extracellular fluid overload, anemia and HTN ↑ myocardial work and O2 demand and accelerated rate of artherosclerosis; Tx: H2O and Na restriction, loop diuretics often in combination with thiazides) |
TX of CV complications associated with chronic kidney disease
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What is the dietary treatment options for chronic kidney disease?
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Protein restriction (studies inconclusive; but ↓ Albumin at start of dialysis is strong predictor of mortality)
Na and H2O restriction (Na intake > 3-4 g/d edema, HTN and CHF, while Na intake < 1 g/d volume depletion and hypotension; 2 g Na/day are recommended w/ fluid intake of 1-2 L/day) K restriction (< 50-60mEq /d) Phosphorus restriction (limit intake of cola, eggs, dairy and meat; add Phosphorus binder if GFR < 20-30ml/min) Magnesium restriction (all laxatives and acids with Mg are relatively contraindicated) |
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What is the dialysis treatment option for chronic kidney disease?
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Start when GFR is 10 ml/min or creatinine is 8 mg/dl (in diabetic 15ml/min and 6 mg/dl respectively)
Indications for Dialysis Refractory ↑ Kalemia Fluid overload unresponsive to diuresis Severe metabolic acidosis (pH< 7.20) Uremic Syndrome (encephalopathy, pericarditis, coagulopathy) Neurologic Sx (seizures or neuropathy) |
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What is the hemodialysis treatment option for chronic kidney disease?
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Arteriovenous fistula w/ constant blood flow along semipermeable membrane and dialysate (cleansing solution) on the other side
Goals: Remove unwanted substances and add back needed components 3x /week, each session lasting 3-5 h |
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What are the details of peritoneal dialysis as treatment for chronic kidney disease?
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Dialysate enters the peritoneal cavity through a catheter
Fluids and solutes move across the capillary bed between the visceral and the parietal layers of the peritoneal membrane CAPD - Continuous ambulatory peritoneal dialysis (pt exchanges dialysate 4-6 x /day) CCPD - Continuous cyclic peritoneal dialysis (cycler machine automatically performs exchange at night) Permits grater patient autonomy Monitor nutritional status since large amounts of albumin are also removed Complication: Peritonitis with staph aureus as most common infecting organism 5 year survival rate: 36% overall, 21% in diabetics |
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What are the details of kidney transplant as treatment for chronic kidney disease?
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2/3 of kidney transplants are cadaver organs
Immunosuppressive drugs With live donor organ 3 yr graft survival rate = 88%; with cadaver organs 3 yr graft survival = 78% Rejection depends on immunologic factors as well as age and race of recipient, donor age, length of time on dialysis and coexisting hyperlipidemia, HTN or cytomegalovirus infection Average wait for a cadaver kidney is 2-5 years |
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What are the three major categories of glomerulonephropathies?
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3 major categories
NephrItic Syndrome NephrOtic Syndrome Asymptomatic renal dz |
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Acute glomerulonephritis
Inflammatory process renal dysfct within days to weeks Sx: Periorbital or scrotal edema, HTN 2/2 volume overload Labs: No specific chemistries UA: dysmorphic RBC, RBC casts and some protein Bx: Type of dz can be categorized according to immunofluorescent pattern and appearance on electron microscopy Tx: BP and fluid overload control, Na and H2O restriction, diuretics, dialysis prn |
Nephritic syndrome
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Postinfectious Glomerulonephritis
Most often 2/2 group A β hemolytic strep Occurs 1-3 weeks after pharyngitis or impetigo Also viral, fungal or parasitic causes possible Sx: Oliguria, edema, HTN Labs: ↑ ASO titers in group A strep infection UA: Cola-colored, RBC, RBC casts and protein < 3.5 g/d |
Nephritic syndrome
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How do you diagnose and treat nephritic syndrome?
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Dx: Immunoflurescence shows IgE and C3 in granular pattern in the mesangium and along the capillary basement membrane
Dx: Large, dense subepithelial deposits under electron microscope Tx: Supportive, Abx, Na restriction, diuresis Prognosis: 5% of adults develop rapidly progressive glumerulonephritis, and few cases progress to ESRD |
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In 1/3 of cases it is 2/2 systemic renal disease such as DM or lupus
Remainder of cases is idiopathic Sx: First peripheral edema 2/2 Na retention (not 2/2 low plasma oncotic pressure) generalized edema UA: Protein > 3.5g/day, few cells or casts, but have oval fat bodies in hyperlipidemia Labs: ↓ serum albumin and total protein Dx: Immunofluorescence and electron microscopy, Bx |
Nephrotic syndrome
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In regards to protein loss and edema how do you treat nephrotic syndrome
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Protein loss
Protein restriction that may decrease glomerulosclerosis ACE-I (reducing glomerular capillary pressure and proteinuria by ↓efferent arteriolar resistance) Edema Na restriction Diuretics (are dependent on protein so large doses are needed; combination of loop diuretics and Thiazides are best) |
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In regards to hyperlipidemia and hypercoagulable state how do you treat nephrotic syndrome?
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Hyperlipidemia
Dietary modification and exercise Pharmacologic management Hypercoagulable State 2/2 to antithrombin 3, protein C and S loss in the urine and ↑ platelet activation lead to renal vein thrombosis Anticoagulation x 3-6 mo, if recurrent Tx indefinitely |
