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75 Cards in this Set

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What are three ways in which to evaluate renal failure?
Estimate duration
UA
Glomerular filtration rate (GFR)
retention of BUN and Creatinine =
Azotemia
What are the specific details of a urine analysis?
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
Hematuria with dysmorphic RBC, RBC casts and protein in the urine analysis.
Glomerulonephritis
Protein and lipids revealed in the urine analysis.
NephrOtic Syndrome
Pigmented granular casts, renal tubular epithelial cells in the urine analysis.
Acute Tubular Necrosis
WBC (neutrophils and eosinophils), WBC casts, RBC and some protein in the urine analysis.
Interstitial Nephritis or Pyelonephritis
Proteinuria =
> 150-160mg/24h in an adult
Significant Proteinuria =
> 1g/24h
NephrOtic-range Proteinuria =
> 3.5g/24h
What are the functional reasons for proteinuria?
Benign, in response to acute illness, or exercise.
What is the reason for overload proteinuria?
Overproduction of circulating filterable plasma proteins such as Bence Jones proteins in multiple yeloma, myoglobin in rhabdomyolysis and Hgb in hemolysis.
What is the reason for glomerular proteinuria?
Increased permeability across glomerular basement membrane (GBM)
What is the reason for tubular proteinuria?
Faulty reabsorption in proximal tubules in e.g. acute tubular necrosis, toxic injury etc.
What is the TX for proteinuria?
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
Hematuria: =
> 3 RBC/ high power field
False + on dipstick in testing for hematuria 2/2?
vitamin C, beets or rhubarb, bacteria or myoglobin
What is the cause of hematuria?
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
What can be seen on ultrasonography with renal failure?
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
What can be seen with intravenous pyelogram with renal failure?
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)
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
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
What are the indications for a renal biopsy?
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
After renal biopsy, what is expected?
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
Sudden ↓ in renal function leading to inability to maintain fluid and electrolyte balance and to excrete nitrogenous wastes (marked by increased creatinine)
Acute Renal Failure
What are the signs and symptoms of acute renal failure?
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)
What are the laboratory findings of acute renal failure?
↑ 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
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
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
Patients with prerenal failure failure have low fractional excretion of?
Na
What is the Tx for prerenal azotemia - acute renal failure?
Depends on cause
Maintain euvolemia
Monitor serum K
Avoid nephrotoxic drugs
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
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
How do you DX/TX Postrenal Azotemia - Acute Renal Failure?
U/S
Bladder catheterization (if hydronephrosis and bladder enlargement)
Then monitor lytes and keep pt hydrated 2/2 postobstructive diuresis
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
What are the three types of intrinsic renal failure?
Acute tubular necrosis

Interstitial nephritis

Glomerulonephritis
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
What are two things responsible for causing acute tubular necrosis?
Exogenous and endogenous nephrotoxins.
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
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
Prevention of renal damage by exogenous nephrotoxin (contrast):
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)
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
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
What are the lab findings for acute tubular necrosis?
‘Muddy brown’ casts
↑ Kalemia
↑ Phosphatemia
What is the TX for acute tubular necrosis?
Avoid fluid overload and ↑ Kalemia
High dose Furosemide (20-160mg po qd) – no affect on mortality
Dialysis
What is the outcome or expectations for acute tubular necrosis?
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!
10-15% of intrinsic renal failure
Mechanism: Interstitial inflammatory response with edema and possible tubular cell damage
Interstitial nephritis - intrinsic renal failure
What are the causes of interstitial nephritis - intrinsic renal failure?
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 )
What are the symptoms of interstitial nephritis - intrinsic renal failure?
Fever
Transient maculopapular rash
Arthralgias
Eosinophelia


Urine: RBC, WBC, WBC casts, proteinuria (especially if caused by NSAIDS), eosinophils
What is the prognosis and expected outcome for interstitial nephritis?
Good prognosis, rarely progresses to ESRD
Worse outcome in oliguric failure and advanced age
Recovery over weeks to months
Tx
Short course of corticosteroids
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
What are the signs and symptoms, lab findings and DDX for glomerulonephritis?
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
What is the TX for glomerulonephritis?
High dose corticosteroids
Cytotoxic agents such as cyclophosphamide
Plasma exchange in Goodpasture dz until chemotherapy takes effect
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
Stage GFR
1 ≥ 90
2 60-89
3 30-59
4 15-29
5 < 15
Chronic Kidney Disease staging
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
What are some symptoms of chronic kidney disease?
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
What are some signs of chronic kidney disease?
HTN, rales, cardiomegaly, edema, pericardial friction rub

Uremic frost

Uremic fetor = fishy odor of the breath
What are the lab findings and the image findings with chronic kidney disease?
Previously ↑ BUN and creatinine
Anemia
Metabolic acidosis
↑ Phosphatemia
↓ Calcemia
↑ Kalemia
Urine: Broad waxy casts

Small bilateral echogenic kidneys on U/S
↑ 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
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
↑ 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
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
What is the dietary treatment options for chronic kidney disease?
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)
What is the dialysis treatment option for chronic kidney disease?
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)
What is the hemodialysis treatment option for chronic kidney disease?
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
What are the details of peritoneal dialysis as treatment for chronic kidney disease?
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
What are the details of kidney transplant as treatment for chronic kidney disease?
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
What are the three major categories of glomerulonephropathies?
3 major categories
NephrItic Syndrome
NephrOtic Syndrome
Asymptomatic renal dz
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
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
How do you diagnose and treat nephritic syndrome?
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
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
In regards to protein loss and edema how do you treat nephrotic syndrome
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)
In regards to hyperlipidemia and hypercoagulable state how do you treat nephrotic syndrome?
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