Test #1 Flashcards
Azotemia
Elevated BUN/Creatinine
The buildup of abnormally large amounts of nitrogenous waste products in the blood
Types of azotemia
Pre-renal failure
Intrinsic renal failure
Post-renal obstruction
Oliguria
Urine output < 400 mL/day
Urine output < 20 cc/hr
Anuria
Urine output < 100 mL/day
Glomerular filtration rate (GFR)
The sum filtering rate of all functioning neurons
-Kidney filtration rate
Measure Creatinine, Urea, or Inulin clearance
GFR Normals by gender
Men = 130 mL/min/173 m2
Women = 120 mL/min/173 m2
Decrease normally w/ age
Influenced by age, sex, body size, and renal blood flow
Creatinine clearance
Assess GFR
Normals: Men = 107-139
-Women = 87-107
Can overestimate the GFR by 40%, especially with decreased renal function
Major body cations and normal values
Sodium: 135-145
Potassium: 3.8-5.5
Major body anions and normal values
Chloride: 98-106
Bicarbonate: 21-28
Total CO2: 23-30
Typically secreted electrolytes
Hydrogen
Potassium
Urate
Odors indicate:
Ammonia-like
Foul/offensive
Sweet
Fruity
Maple syrup-like
Ammonia-like: Urea-splitting bacteria
Foul/offensive: Old, pus, inflammation
Sweet: Glucose
Fruity: Ketones
Maple syrup-like: Maple syrup urine disease
Colors indicate:
Colorless
Deep yellow
Yellow-green
Red
Brownish-red
Brownish-black
Colorless: Dilute urine
Deep yellow: Concentrated urine
Yellow-green: Bilirubin
Red: Blood/Hemoglobin
Brownish-red: Acidified blood (acute glomerulonephritis)
Brownish-black: Homogentisic acid (Melanin)
Globulinuria DDx
Glomerulonephritis
Tubular dysfunction
Bence Jones proteinuria DDx
Multiple myeloma
Leukemia
Fibrinogen proteinuria DDx
Severe renal disease
Types of ketone bodies
Acetoacetic acid
Acetone
Betahydroxybutyric acid (most common)
Nephrotic syndrome vs nephritic syndrome
Lots of protein loss w/ nephrotic
Lots of blood loss w/ nephritic
Acute renal failure
Heath’s intro
Abrupt kidney function loss w/in 7 days
Pre-renal, intrinsic, or post-renal
Chronic kidney disease
Heath’s intro
Progressive renal function loss over months/years
End-stage renal disease
Heath’s intro
Chronic kidney disease at stage 5 progression
GFR <15
Glomerulopathy
Heath’s intro
Disease of glomeruli or nephron
Can be inflammatory or non-inflammatory
Nephritic syndrome, IgA nephropathy, Nephrotic syndrome
Hydrostatic vs osmotic pressure
Hydrostatic pressure pushes fluid into the interstitium
Osmotic pressure pushed fluid from interstitium back into capillary/tubule
Fluid and electrolyte intake and output regulation
Fluid intake - hypothalamus regulates thirst
Electrolyte intake - dietary habits regulate
Output of both is regulated by kidneys
Mechanisms to stimulate hypothalamic thirst center
Increased plasma osmolality (Dry mouth and osmoreceptors stimulated)
Decreased plasma volume (RAAS and decreased BP)
ADH stimulation and mechanism
Stimulated by dehydration, increase in osmolality, or RAAS
Increases water absorption by increasing the number of aquaporins in the collecting tubule
Kidney blood vessel order
Aorta - renal artery - segmental artery - interlobar artery - arcuate artery - cortical radiate artery - afferent arteriole - glomerulus
Glomerulus - efferent arteriole - peritubular capillaries and vasa recta - cortical radiate vein - arcuate vein - interlobar vein - renal vein - inferior vena cava
Renal clearance
Volume of plasma completely cleared of waste by kidneys per minute
Clearance = (Urine concentration * urine flow rate) / plasma concentration
Can be used to estimate GFR if substance excreted is freely filtered w/o absorption
Renal autoregulation
Allows GFR to remain stable in spite of arterial blood pressure changes
Afferent and efferent arterioles change resistance to modify GFR and blood flow
Myogenic response and tubuloglomerular feedback (macula densa)
Feedback that triggers an increase in GFR
Prostaglandins
Fever/pyrogens
Glucocorticoids
Hyperglycemia (DM)
Macula densa senses low NaCl
Feedback that triggers a decrease in GFR
NSAIDs
Aging (10% decline/decade after 40 years)
PCT
Most reabsorption of vital substances - glucose, aa, bicarb, Na, Cl, water
Ammonia is generated and secreted here
Mannitol and acetazolamide diuretics work here
Angiotensin II increases sodium and water reabsorption
PTH increases phosphate excretion
Transport maximum
Some substances (glucose) can only be absorbed to a certain threshold, and all excess gets excreted
Loop of Henle - thin descending loop
Water is passively absorbed here
Loop is impermeable to sodium and solutes (medulla hypertonicity)
Loop of Henle - ascending loop
Not permeable to water, but active electrolyte reabsorption occurs here w/ Na/K/Cl pump
Loop diuretics (Lasix) work here to shut down pump and produce very dilute urine
The high osmotic gradient created here allows for urine concentration later
DCT
Subjected to hormonal control (Aldosterone, ADH, Angiotensin II, ACEI, ANP)
Early DCT only electrolytes permeable
Late DCT and CT - ADH controls water permeability
-principal and intercalated cells assist w/ concentration here
Aldosterone
Secreted from adrenal gland
Increases sodium absorption and potassium secretion in order to maintain blood volume and pressure
Triggered by RAAS
Angiotensin II
End of RAAS
Causes Aldosterone, ADH release
Also causes arterial constriction, increases GFR and increases thirst
Results in BP increase, water retention, and increased fluid intake
ACEI/ARB effect on kidneys
Inhibits RAAS - decreased aldosterone and ADH secretion
Decreases efferent arteriolar resistance and directly inhibits sodium reabsorption
Results in natriuresis, diuresis, and decreased BP
ANP
Secreted by atrial BP increase
Inhibits sodium and water reabsorption to reduce BP and volume
Inhibits RAAS while increasing the GFR
Common secreted by the tubule
Bile salts
Oxalate
Urate
Creatinine
Catecholamines
Collecting duct
Concentrates the urine according to the ECF osmolality and ADH levels
Cockcroft-Gault Formula
GFR/CrCl = [(140-age)*kg] / (72-SCr)
Multiply by 0.85 for women
MDRD
Takes gender and race into account for eGFR
Normal: >60mL/min/1.73 m2
Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)
Measure creatinine w/ external filtration markers in order to provide a more accurate eGFR in patients w/ normal/mildly reduced GFR
BUN
Normal: 6-20 mg/dL
Waste of protein breakdown - urea that becomes BUN as soon as its in the blood
Increased BUN DDx
Renal disease
Excess protein breakdown
High protein diet
GI bleed
Decreased BUN DDx
Liver disease
Starvation
Creatinine
Muscle breakdown byproduct
Normal: 0.8-1.4 (men) 0.6-1.2 (women)
Steady-state relationship w/ GFR
Used w/ BUN to distinguished types of azotemia
Increased Creatinine DDx
Renal failure
High protein diet
Meds (ACEI, NSAIDs, diuretics)
Muscular disease
Decreased Creatinine DDx
Pregnancy - normal effect 0.4-0.6 mg/dL
Occurs because GFR and volume increase
Creatinine and BUN filtration dynamics
BUN can be absorbed over time w/ a decreased GFR
Creatinine is not absorbed, is secreted into CT for excretion
-Any Creatinine increase may be caused by blocked secretion (cimetidine (antacid, antihistamine), trimethoprim (Bactrim)
BUN:Creatinine increases
Both should increase proportionally to indicate intrinsic or post-renal disease
Increased BUN w/ normal creatinine DDx
Pre-renal azotemia
Catabolic state (increased breakdown)
GI bleed
High protein diet
Drugs (tetracyclines, steroids)
Decreased BUN:Creatinine DDx
ATN
Low protein/starvation
Liver disease
Dialysis
SIADH
Pregnancy
Decreased BUN w/ Increased Creatinine DDx
Rhabdomyolysis
Muscular patient in renal failure
Hyponatremia DDx and treatment
Volume overload
Excess sodium and water loss
Tx: sodium and water replacement, treat underlying cause
Hypernatremia DDx and Treatment
Excessive water loss -> dehydration
Tx: Fluid replacement w/ diuretics to eliminate excess sodium
Hypochloremia DDx
GI upset
DKA
Mineralocorticoid excess
Salt-losing renal disease
High bicarbonate levels
Calcium normal levels
8.5 - 10.5
Magnesium normal levels
1.4 - 2
Sodium normal levels
135-145 mmol/L
Potassium normal levels
3.5-5.5 mmol/L
Chloride normal levels
96 - 106
Phosphorus normal levels
2.0 - 4.5
Glucose normal levels
80-120 mg/dL
Hyperchloremia DDx
Metabolic acidosis
GI loss
Mineralocorticoid deficiency
Urine Chemical analysis
Glucose
Bilirubin
Ketones
Specific gravity
Blood
pH
Protein
Urobilirubin
Nitrite
Leukocyte esterase
Specific gravity
Normal: 1.010-1.025
Indicates degree of urine concentration/dilution
Low: Diabetes insipidus, tubular/renal damage, well-hydrated
High: DM, adrenal insufficiency, hepatic disease, CHF, excessive water loss
Urine pH
Normal: ~6
Low: high protein diet, meds, DKA/metabolic acidosis
High: Post-prandial, high veggie/dairy diet, meds, UTI (depends on organism)
Urine Protein
Single most important indicator of kidney disease
Can also be benign - functional changes or orthostatic (adolescents)
Urine Glucose
Shows up when maximum threshold is reached (>180)
Investigate for diabetes
May be benign - renal glycosuria from heavy meals or emotional stress
Urine Ketones
Fatty-acid metabolism
Betahydroxybutyric acid most common
DDx: DKA, restrictive carb diet/starvation
Urine Bilirubin
Indicates liver disease
- Hepatocellular disease
- Biliary obstruction
- Increase in conjugated (direct) bili
Urine Urobilinogen
Converted from bilirubin in the intestinal tract
Indicates liver problem, rules out bile duct obstruction if present
DDx: hepatitis, cirrhosis, CHF, pernicious anemia
Urine blood
Hematuria (rbc intact): renal disease, infection, neoplasm, trauma
Hemoglobinuria: same as hematuria + transfusion reaction, anemia, burns, poisoning
Urine Leukocyte esterase
Released into urine by neutrophilic granulocytes
Indicates pyuria, bacteriuria, UTI
Urine Nitrate
Nitrate reduced by G(-) bacteria
Indicates infection, usually E. coli
RBC casts
Indicates kidney is bleeding, either from vascular insult or parenchyma breakdown
Acute inflammatory or vascular disorder
May be only manifestation of acute glomerulonephritis
WBC casts
Indicate kidney inflammation/infection
DDx: Acute pyelonephritis, interstitial nephritis, proliferative glomerulonephritis
Hyaline casts
Non-specific
Get with concentrated urine or diuretic therapy
Granular casts
Leakage and aggregation of protein
Coarse, deeply pigmented granular casts = ATN
Waxy casts
Last stage of granular cast degeneration
Non-specific, any variety of acute or chronic kidney disease
KUB
Used to look for kidney stones
Low radiation, inexpensive
Not all stones show up
Sonography applications for kidney
Characterize renal mass
Detect obstruction or hydronephrosis
Polycystic kidney disease or renal failure (structural/functional abnormalities)
Cannot see ureters
IVP indications
Really only used for obstruction or hematuria
Medullary sponge kidney
Papillary necrosis
Stones in the ureter
CT scan
Gold standard for kidney stones and diagnosis renal tumors
Renal Arteriography
Gold standard for renal artery stenosis
Renal venography
Used to diagnose renal vein thrombosis
Retrograde/Anterograde Pyelography
For diagnosis of urinary tract obstruction or tumors
CT and US are more commonly used
Hypovolemic hyponatremia DDx and Tx
GI or renal loss
Tx: NS with a possible slow bolus and maintenance if ongoing loss
Normovolemic hyponatremia DDx
SIADH
Primary polydipsia
Low dietary sodium
Hypervolemic hyponatremia DDx and Tx
CHF
Cirrhosis
Kidney disease
Nephrotic syndrome (rare)
Tx: restrict fluids and sodium (1000-1200 mg/day)
-Loop diuretics to removed excess fluid, watch potassium carefully
Hyponatremia and serum osmolality
Isotonic: Hyperproteinemia, hyperlipidemia
Hypotonic: Determine volume status
Hypertonic: Hyperglycemia, radiocontrast agents, Mannitol/Sorbitol/Glycerol/Maltose
Chronic Hyponatremia
Cerebral adaptation
Sx: Fatigue, nausea, dizziness, confusion, lethargy, muscle cramps, gait issues, forgetfulness
Acute hyponatremia
Acute hyponatremic encephalopathy
Cerebral effects depend on degree of hyponatremia
Fatigue/malaise followed by HA, lethargy, coma, seizures
Eventual respiratory arrest
Causes permanent neurological damage or death
SIADH and treatment
Get volume depletion and decreased tissue perfusion
Treat underlying cause, fluid restriction w/ oral salt tablets and loop diuretics if hypervolemic
Severe Hyponatremia Tx
@ high risk for brain herniation
3% hypertonic saline w/ hourly sodium checks - increase sodium by 4-6 mEq/L in 24 hours
Cause osmotic demyelination if corrected too quickly, careful w/ high risk pts (acute post-op, hyperacute hyponatremia, or intracranial pathology)
Acute Hypernatremia
Rapid brain volume decrease causes cerebral brain rupture and cause intracerebral/subarachnoid brain hemorrhage
Can occur with overly rapid correction of chronic hyponatremia = brain demyelination
Chronic Hypernatremia effects
Brain adapts w/in 1 day by pulling water from CNS and increasing cell solute uptake (increases water in cells)
Most who get this already have an existing neurological disease that diminishes thirst
Hypernatremia Treatment
Free water (D5W) + NS if hypovolemic
Decrease serum sodium slowly, monitor closely and calculate total body water replacement
Diabetes Indipidus
Central: not enough ADH produced
-Tx: Desmopressin and fluid restriction
Nephrogenic: kidneys are resistant to ADH
-Tx: Thiazide and sodium restriction
Hypercalcemia
Cause: cancer, primary hyperparathyroidism, drugs (thiazide, lithium)
EKG: Short QT interval
Sx: N/V, polyuria/polydipsia, neuro or psych sx
Causes oliguric renal failure, coma, V-arrhythmias, death
Hypercalcemia tx
NS and loop diuretics
Drop 2-3 mL in 24-48 hrs
Bisphosphonates (if malignant), Osteoclast inhibitors, dialysis
Hypocalcemia
Causes: Hypoparathyroidism, Vitamin D deficiency, loop diuretics, phosphates
Sx: tetany, QT prolongation, mouth paresthesias, decreased myocardial contractility
Hypocalcemia Tx
Calcium salts IV over 5-10 minutes for less than 60 minutes
-Use gluconate if in a peripheral vein
Chronic hypocalcemia: Oral Ca supplements, 1-3 ELEMENTAL grams/day
-Add 1000 Vitamin D if no response
SE: Constipation, GI
Hyperphosphatemia
Decreased excretion w/ low GFR, chemo, rhabdo
Can be chronic w/ hypocalcemia
Tx: GI binders w/ IV Ca salts, dialysis and dietary restrictions
-avoid aluminum-containing antacids (cause bone dx)
Hyperphosphatemia
Usually asx until <1.0
Long-term: proximal muscle weakness and osteomalacia
Tx: Severe - Slow IV phosphorus
Mild/moderate - oral phosphates (250mg)
SE: GI upset
Hypomagnesemia
Cause: Increased excretion, impaired absorption, or reduced intake, drugs (diuretics, aminoglycosides, ETOH)
Sx: Neuromuscular (cramps, tetany), calcium metabolism inhibited
EKG: Widened QRS, AF, VT, VF
Hypomagnesemia Tx
Only treat if symptomatic or <1.0
IV MgSO4 - bolus and maintenance
-SE: Flushing, sweating
Oral tx if mild/moderate - sustained release
-SE: Diarrhea
Hypermagnesemia
Sx worse as Mg increases - can cause cardiac or respiratory arrest
Tx: IV calcium to antagonize neuro and CV effects
- Renal failure: dialysis
- Normal kidneys: forced diuresis w/ fluid and loop diuretics
Hypokalemia
Cause: beta-2 agonists, loop diuretics/thiazide, ACEI, PCN, ampho B, Insulin, metabolic acidosis, V/D
EKG: U wave w/ inverted T waves
Hypokalemia Tx
Loop/thiazide-induced: 40-100 mEq potassium supplements PO
Severe/sx: IV potassium in NS, dextrose to shift K into the cells
-Monitor on EKG, have to give lower dose through a peripheral line
Hyperkalemia
Cause: increased intake, decreased excretion, Aldosterone resistance, shift to ECF
Sx: Ascending muscle weakness
EKG: Peaked T waves w/ shortened QT initially, progress to long QRS and QT with P wave loss -> dysrhythmias
Hyperkalemia Tx
Stabilize cardiac w/ calcium gluconate IV
D5W to shift potassium back into the cell
Bicarb if acidotic
Dialysis and K+ binders w/ renal failure
Consider a loop diuretic
Hypotonic crystalloids
Lower osmotic pressure than blood
Shift fluid into cells and interstitium
D5W (once injected), 1/2 NS
Dont use w/ suspected brain injury, liver disease, trauma, or burns
Hypertonic crystalloids
Volume expanders
7.5% NS, Dextrose, D50
Higher osmotic pressure - draw fluid into intravascular
For severe hyponatremia, cerebral edema
Cause fluid overload and pulmonary edema
Maintenance therapy
Daily weights to monitor
Account for obligate fluid loss (1600)
0.45% NS + 20 mEq KCl
For fever >37, increase in 100-150 water needs
4/2/1 degree rule to calculate maintenance flow rate
Drugs that do not need adjusting for renal failure
Azithromycin
Ceftriaxone
Moxifloxacin
Doxycycline
Replacement therapy treatment (hypovolemia)
Reduced intake/excess excretion - 0.45% then 0.25% if Na>145, 0.9% if Na<138
V/D - 0.9% until labs
Hemorrhage/burn - 1-2 L wide bore IV, consider PRBC/Albumin
Hydrate until urine production >30 mL/hr occurs
Resuscitation (hypovolemic shock)
Severe - 1-2L 0.9% rapid infusion
Mild/moderate - 50-100 L/hr then replace loss
May cause fluid overload, be careful and look for signs
Colloids
Draw fluid into intravascular space
Less volume required and longer duration of action than hypertonic crystalloids
5% Albumin
Hydroxyethalstarches
5% Albumin
Volume expansion, protein replacement, hemodynamic stability in shock
CI: Anemia, heart failure, sensitivity, ACEI w/in 24 hours (flushing, hypotension)
When to use D5W alone
Only if pt Na >145 and symptomatic of hypernatremia
Uremia symptoms
Fishy breath odor
Metallic taste in mouth
Erectile dysfunction
Retrosternal pain w/ inspiration
Restless legs
Numbness
Cramps
CKD comorbidities/complications
Anemia
Bone/mineral abnormalities
CV and renal risk
Diabetes
Dialysis indications
Hyperkalemia
Metabolic acidosis
Pericarditis
Pre-transplant immunosuppression
Steroids - 5mg/kg
Mycophenolate mofetil - 500-1000 mg BID
Basiliximab - 20mg 1 hour before transplant
Gancyclovir and broad spectrum Abx prophylaxis
Transplant rejection diagnosis
Serial creatinine measurements
>20% over baseline
Rule out non-immunologic causes
CKD vaccinations
H1N1
Hepatitis A and B
Influenza
Pneumococcal (PPV)
Criteria for a benign cyst
- Echo free on US
- Sharply demarcated
- Enhanced back wall on US - fluid free of cells
Follow up in 6 months if cyst is benign
Autosomal dominant polycystic kidney disease treatment
Treat HTN and manage infections
-Bactrim, Chloramphenicol, Ciprofloxin
Dialysis and transplant w/ ESRD
Bilateral nephrectomy w/ recurrent UTIs
PKD history symptoms
Family history
History of stones/UTIs/Pyelonephritis
HTN
Abdominal masses
Autosomal recessive polycystic kidney disease treatment
Manage HTN, UTIs - probably w/ constant Abx prophylaxis
Diet supplements, growth hormone
Dialysis/transplant
Acquired cystic kidney disease
Cysts in dialysis pts w/ CKD/ESRD
Screen pts who have been on dialysis 3-4 yrs
CT scan for Dx
Medullary cystic disorders
Occurs in kids - can’t potty train, excessive thirst
-low BP, failure to thrive
Causes ESRD in childhood
Tx: liberal fluid/sodium intake
-manage renal failure, dialysis
Transplant these kids
Medullary sponge kidney
Bunch of grapes/ bouquet of flower on CT/IVP
Pts w/ kidney stones
Renal failure doesn’t occur
Tx: manage UTIs and stone formation
When do you calculate the GFR
When Scr > 1.5 or the pt is >65 yo
Nephrotoxic agents
NSAIDs
Aminoglycosides
Heavy metals
Radiocontrast agents
Ethylene glycol (antifreeze, oxalic acid + Ca deposits throughout body)
Dosing modification guidelines
Need adjustments when GFR < 10 or 10-50
Unless otherwise indicated, not needed when GFR > 50
