Clinical Medicine 9/20/16--Kirila Flashcards
Acute Kidney Injury
- increase in serum creatinine +/- decrease in urine output over hours to days
- electrolyte disturbances, acid-base disturbances (metabolic acidosis), inability to excrete nitrogenous waste, intravascular volume overload
Orthostatic hypotension
- volume contraction or ECV depletion (dehydration)
- due to fluid losses from nausea and vomiting
Fractional excretion of sodium
- calculated using a random urine sample close to time of the blood draw–helps sort between pre-renal and intrinsic renal
- (Una/Pna)/(Ucr/Pcr)x100
FeNa less than 1% means
tubules intact and are sodium avid i.e. retaining sodium as would be expected in dehydration
FeNa greater than 1-2% means
tubular function not intact
Pre-renal origin suggests
-that the tubules and glomeruli were not the initial location of pathology, though they will eventually become affected and possibly permanently
BUN/Creatinine in AKI
- elevation in serum Creatinine by 50% or by 0.5-1.0mg/dL (affected by muscle mass available to generate creatinine)
- BUN also elevated due to retention of nitrogenous wastes
Elevated BUN=
azotemia
Elevated BUN plus confusion=
uremia
eGFR=
175x (serum creatinine)^-1.154x(age)x0.742 [if female] x 1.22 [if black]
Pre renal causes of acute kidney injury
- anything that compromises renal perfusion
- hypovolemia: dehydration, viral syndromes, acute pancreatitis, diuretics
- low cardiac output: CHF
- altered renal/SVR ratio: sepsis, cirrhosis
- renal hypo perfusion with impaired autoregulation: NSAIDS
- hyperviscosity syndrome (rare): myeloma
- not something that started in the kidney! Something before you got to the kidney
Effective Volume depletion
- 3rd space
- results in decreased kidney perfusion as seen in pre-renal disease
Pre renal treatment
- hypovolema: fluid replacement IV; treat underlying cause
- even with effective volume depletion such as pancreatitis, large quantities of IV fluids are indicated, with close monitoring for systemic volume overload
Intrinsic renal failure
- renovascular obstruction: renal artery obstruction e.g. embolism, dissecting aortic aneurysm (can be pre renal or intrinsic renal)
- disease of glomeruli or microvasculature: accelerated HTN
- acute tubular necrosis: iodinated contrast dye–used with CTs, vascular studies, IVP’s, etc
- interstitial nephritis: acute pyelonephritis, NSAIDs, also can be contrast dye induced, other drugs
- intratubular deposition and obstruction: myeloma
- renal allograft rejection
Post renal AKI
-blockage
Ureteric blockage
-calculi (stones), blood clot, sloughed papilla, cancer, external compression (tumor, retroperitoneal fibrosis)
Bladder neck blockage
-neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clots
Urethra blockage
-stricture, congenital valve, phimosis
If AKI unresponsive to conservative measures,
- consider temporary hemodialysis in the following:
- volume overload refractory to diuretics
- hyperkalemia
- encephalopathy otherwise unexplained
- pericarditis, pleuritis
- severe metabolic acidosis comprising respiratory or circulator function
Chronic Kidney disease
- long-standing, irreversible impairment of renal function
- uremia: clinical syndrome resulting from profound loss of renal function
Glomerular filtration rate
- Creatinine clearance: 24 hour urine sample measured for creatinine in addition to obtaining serum creatinine
- can use inulin as substance to measure, but has to be given IV and assay for inulin not available in most labs
CKD Stage 1
-kidney damage with normal or increased GFR>or = 90
CKD Stage 2
-mild decrease in GFR
60-89
CKD Stage 3
moderate decrease in GFR
-30-59
CKD Stage 4
Severe decrease in GFR
-15-29
CKD Stage 5
kidney failure (aka ESRD)
Early stage of CKD
- usually symptom free
- overall function intact
- reserve function diminished
- BUN/Cr may even be in normal range
Later stages of CKD
- azotemia and accompanying symptoms/signs
- reserve decrease sufficiently so sudden stress can induce further compromise: infection, urinary obstruction, dehydration, nephrotoxic drugs
Effects of Uremic Toxins on Cellular Function
- reduction in transmembrane voltage
- increased intracellular Na+
- decreased intracellular K+
- inhibition of Ca+ flux
- uremia and its effects are largely reversible with dialysis
- normal erythrocytes incubated in uremic serum demonstrates similar changes
Effects of Uremic Toxins on Whole Body Composition
- osmotically induced over hydration of cells
- increased extracellular volume
- malaise, anorexia, N/V/D
- protein and calorie malnutrition
- negative nitrogen balance
- profound loss of lean body mass and fat deposits
Effects of Uremic Toxins on Metabolism
- hypothermia (decreased Active Na+ transport)
- intracellular deficits of K+
- metabolic acidosis
Effects of Uremic Toxins on Nitrogen and Lipids
- protein intolerance
- increased catabolism in uremia
- decreased elimination
- hypertrigliceridemia, decreased HDL, normal cholesterol
- decreased removal by lipoprotein lipase
- increased lipogenesis
- possibly increased production by liver and intestine
Effects of Uremic Toxins on sodium and volume homeostasis
- total body content of Na+ and water are increased modestly–in stable CKD
- excessive salt ingestion can lead to: CHF, hypertension, ascites, edema
- excessive water ingestion: hyponatremia; weight gain
- recommended fluid intake pre-dialysis: urine output plus 500ml/day
Potassium effects in chronic renal disease
- normal until late stages: adaptation in renal distal tubule and colon=sites where aldosterone enhances K+ secretion
- increased K+–cardiac arrhythmias
Drugs that can increase serum potassium
- antikaliuretic drugs: spironolactone, triamterene, amiloride, trimethoprim, pentamidine
- others: ACE inhibitor, beta blockers
Extra renal Fluid loss also contributes to CKD
- impaired renal mechanism to conserve Na+ and water in CKD
- vomiting, diarrhea, fever
- –volume depletion: dry mucous membranes, dizziness, syncope; tachycardia, decreased JVP; orthostasis; cardiovascular collapse
The most common complication of ESRD
- hypertesion as a result of primary renal disease or effects on kidney from systemic disease
- chronic dialysis patients also have a higher incidence of accelerated atherosclerosis which contributes to the HTN
If no HTN on clinical exam of ESRD patient, consider additional factors:
- salt wasting form of renal disease causing CKD: polycystic or medullary cystic disease; chronic tubulointerstitial disease; papillary necrosis
- volume depletion
- on antihypertensive therapy at the time
Associated conditions with CKD: pulmonary congestion
- unique form–even in absence of volume overload
- normal or mildly elevated intracardiac or pulmonary capillary wedge pressures
- CXR: butterfly wing distribution (peripheral vascular congestion)
- increased permeability of alveolar capillary membranes
Associated conditions with CKD: pericarditis
- less frequent with early dialysis–thought secondary to metabolic toxins
- if occurs in well dialyzed, likely viral infection or systemic disease
- effusion often hemorrhagic
- treatment: pericardiocentiusis, pericardiectomy
Associated Conditions with CKD: hematologic–abnormal hemostasis
- prolonged bleeding time
- decreased platelet factor III activity
- abnormal platelet aggregation and adhesiveness
- impaired prothrombin consumption
Associated Conditions with CKD: anemia
- normocytic, normochromic anemia
- hemolysis–uremic patients
- GI, chronic dialyzer blood loss
- hypersplenism–occasional
Associated Conditions with CKD: enhanced susceptibility to infection
- lymphocytopenia
- atrophy of lymphoid structures
- neutrophil production relatively unimpaired
- uremia impairs function of all leukocytes
Bone changes with uremia
- renal rickets–widened osteoid seams at growth margins
- osteitis fibrosis cystica–due to secondary hyperparathyroidism: stochastic bone resorption; subperiosteal erosions; terminal phalanges
- osteosclerosis
Bone Changes in Long Term Dialysis
- adynamic or aplastic bone disease
- aluminum-induced osteomalacia
- dialysis-related amyloidosis (DRA)
- -carpal tunnel syndrome; tenosynovitis of hands; shoulder arthropathy; bone cysts; cervical spondyloarthropathy; cervical pseudo tumors
FSGS
- progresses to CKD in 5-10 years
- no proven therapy–may see trial of steroid +/- cytotoxic agent
Signs and symptoms of CKD
- severity depends on: magnitude of loss in renal function
- rapidity of loss
- anorexia
- weight loss
- dyspnea
- fatigue
- pruritis
- sleep and taste disturbance
- confusion, possibly other forms of encephalopathy
CKD Physical Exam findings
- hypertension
- JVD
- pericardial +/or pleural friction rub
- muscle wasting
- asterixis
- excoriations and ecchymoses
CKD Lab findings
- potassium, phosphate, uric acid all high
- calcium, albumin, hemoglobin all low
- metabolic acidosis
Conservative Treatment for CKD
- aggressive control of hypertension
- eliminate volume overload (diuretics, volume intake restriction)
- EPO (rHuEPO)–recombinant human erythropoietin
- phosphate binders–Ca carbonate or acetate
- restrict dietary potassium
- sodium polystyrene sulfonate binds potassium
- Ace inhibitors: diabetes significant protein uria (>1 gm/day)
- dietary protein restriction
Indications for Dialysis
- unresponsive to conservative measures
- volume overload refractory to diuretics
- hyperkalemia
- encephalopathy otherwise unexplained
- pericarditis, pleuritis
- severe metabolic acidosis compromising respiratory or circulatory function
- needs for fluids/drugs also a consideration
Dialysis methods
-Peritoneal dialysis cycler vs dwell time then drain
Intermittent hemodialysis
- most common type used for AKI
- many CKD patients maintained on 3x/week
Night time dialysis
- in-center hemodyalisis
- in-home hemodialysis
CRRT (Continuous renal replacement therapy)
- if intolerant to intermittent hemodialysis
- may see in extremely unstable ICU patients
Peritoneal Dialysis Complications
- peritonitis
- hyperglycemia
- hypertriglyceridemia
- obesity
- hypoproteinuria
- dialysis-related amyloidosis
- insufficient clearance due to vascular disease or other factors
Hemodialysis complications
- hypotension
- accelarated vascular disease
- rapid loss of residual renal function
- access thrombosis
- access or catheter related sepsis
- dialysis-related amyloidosis
- protein-calorie malnutrition
- hemorrhage
- dyspnea/hypoxemia
- leukopenia
Renal Transplant ABSOLUTE Contraindications
- active glomerulonephritis
- active bacterial or other infection
- active or very recent malignancy
- HIV
- Heb B surface antigenemia
- Severe comorbidity (vascular disease)
Renal Transplant RELATIVE Contraindications
- age>70 years
- severe psychiatric disease
- moderately severe degrees of comorbidity
- Hep C with chronic hepatitis or cirrhosis
- noncompliance with dialysis or other treatment
- primary renal diseases: primary focal sclerosis with prior recurrence in transplant; multiple myeloma; amyloid; oxalosis
Renal Transplant Complications
- rejection
- immunosuppression: infection, neoplasm
