Acute / Chronic Renal Failure Flashcards
a designation for a heterogeneous group of conditions that share common diagnostic features: specifically, an increase in the blood urea nitrogen (BUN) concentration and/or an increase in the plasma or serum creatinine (SCr) concentration, often associated with a reduction in urine volume
Acute Kidney Injury (acute renal failure)
True or false: its possible to have AKI without injury to the kidney parenchyma
TRUE
Some causes of community-acquired AKI
Volume depletion
Medications
Urinary Tract Obstruction
Some causes of hospital-acquired AKI
Sepsis
Major surgical procedures
Heart/Liver failure
IV iodinated contrast
Medication
3 categories of AKI
Prerenal Azotemia, Intrinsic, Postrenal
Most common form (broad) of AKI
Prerenal Azotemia
A rise in SCr or BUN concentration due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration.
Prerenal Azotemia
Main causes of pre renal azotemia
Hypovolemia
Decreased cardiac output
Liver failure
- low protein = low osmotic pressure
NSAIDs, ACE-I / ARB, Cyclosporine (mess w renal autoregulation)
What might prolonged periods of renal azotemia lead to?
Ischemic injury (acute tubular necrosis)
True or false: pre renal azotemia is reversible
TRUE - reversible once hemodynamics restored
Urinalysis in prerenal azotemia
Essentially normal, maybe a few hyaline casts
Urinalysis in postrenal failure
Essentially normal, maybe a few hyaline casts
Urinalysis in intrinsic renal failure
granular casts, WBC casts, RBC casts, proteinuria, tubular epithelial cells
General symptoms of AKI
N/V/D Pruritis drowsiness / dizzy hiccups SOB anorexia hematochezia
A distended bladder, costovertebral angle tenderness, or enlarged prostate indicate which cause of AKI
Postrenal
Evidence of volume depletion
Tachycardia
Hypotension (absolute or postural)
Low JVP
Dry mucous membranes
Elevated BUN/Cr Ratio - above 20:1
Urine sodium < 20 mEq/L
FeNa <1%
Hyaline casts in urine sediment, possible
Prerenal azotemia
Decreased BUN/Cr Ratio < 15:1
Increased Urine sodium > 40
FeNa > 1-2%
Intrinsic renal causes
When short term dialysis is indicated for AKI
When SrCr > 5-10 mg/dL
Unresponsive acidosis
Electrolyte disorders
Fluid overload
Uremic complications
Most common causes of Intrinsic AKI
Sepsis
Ischemia
Nephrotoxins (endogenous / exo)
Exogenous nephrotoxins
Aminoglycosides
Cisplatin
Amphotercin
Iodinated Contrast
Endogenous nephrotoxins
Hemolysis
Rhabdomyelosis
Myeloma
Intratubular crystals
Intrinsic AKI - Vascular causes
Vasculitis
Malignant HTN
TTP-HUS
Cardiac output and O2 consumption of kidneys
20% of cardiac output
10% of resting O2 consumption
Ischemia associated AKI
Systemic hypotension, coupled with risk factors:
- sepsis
- limited renal reserve (CKD, older age)
Urine sediment with granular casts, renal tubule epithelial cells
Ischemia associated AKI (ATN)
Nephrotixic tubular injury
Common causes of post renal / obstructive AKI
Bladder neck obstruction
(prostatitis, neurogenic bladder, anticholinergics)
Obstructed foley catheters
Clots
Calculi
Urethral strictures
Diagnostic definition of AKI
a rise from baseline of at least 0.3 mg/dL within 48 h
or at least 50% higher than baseline within 1 week,
or a reduction in urine output to less than 0.5 mL/kg per hour for longer than 6 h.
** Serial blood tests showing continued substantial rise of SCr represents clear evidence of AKI **
Radiologic studies that indicate CKD (as opposed to AKI)
Small, shrunken kidneys with cortical thinning on renal ultrasound
Evidence of renal osteodystrophy
Laboratory studies that indicate CKD (as opposed to AKI)
Normocytic anemia in the absence of blood loss
Secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia
A history of prostatic disease, nephrolithiasis, or pelvic or paraaortic malignancy would suggest the possibility of
Postrenal AKI
Physical signs of orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes are often present in
Prerenal AKI
_____ should be suspected in the setting of vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs.
Prerenal AKI
Colicky flank pain radiating to the groin suggests
Acute ureteric obstruction
Nocturia and urinary frequency or hesitancy can be seen in
Prostatic disease
Abdominal fullness and suprapubic pain can accompany
Massive bladder enlargement
Definitive diagnosis of obstruction requires
Radiologic investigations
Idiosyncratic reactions to a wide variety of medications can lead to
Allergic interstitial nephritis
Allergic interstitial nephritis may be accompanied by
fever, arthralgias, and a pruritic erythematous rash.
AKI accompanied by palpable purpura, pulmonary hemorrhage, or sinusitis raises the possibility of
Systemic vasculitis with glomerulonephritis
Complete anuria early in the course of AKI is uncommon except in the following situations:
complete urinary tract obstruction,
renal artery occlusion,
overwhelming septic shock,
severe ischemia (often with cortical necrosis)
severe proliferative glomerulonephritis
vasculitis
Extremely heavy proteinuria (“nephrotic range,” >3.5 g/d) can occasionally be seen in
glomerulonephritis, vasculitis, or interstitial nephritis (particularly from NSAIDs)
If the dipstick is positive for hemoglobin but few red blood cells are evident in the urine sediment,
Rhabdomyelosis, hemolysis
AKI from ATN due to ischemic injury, sepsis, or certain nephrotoxins has characteristic urine sediment findings:
pigmented “muddy brown” granular casts and tubular epithelial cell casts. These findings may be absent in more than 20% of cases, however
Electrolyte imbalances seen in AKI
Hyperkalemia
Hyperphosphatemia
Hypocalcemia
Anion gap is ____ in uremia
often increased - due to retention of anions such as phosphate, hippurate, sulfate, and urate
Low anion gap may provide a clue to the diagnosis of
Mulitple myeloma (presence of unmeasured cationic proteins)
Laboratory blood tests helpful for the diagnosis of glomerulonephritis and vasculitis include
depressed complement levels
high titers of antinuclear antibodies (ANAs)
(SLE)?
antineutrophilic cytoplasmic antibodies (ANCAs)
(Vasculitis)
antiglomerular basement membrane (AGBM) antibodies (Goodpastures)
cryoglobulins.
Enlarged kidneys in a patient with AKI suggests the possibility of
Acute interstitial nephritis
Kidney biopsy considered when
the cause of AKI is not apparent based on the clinical context, physical examination, laboratory studies, and radiologic evaluation
Most often used when glomerulonephritis, vasculitis, interstitial nephritis, myeloma kidney, HUS and TTP, and allograft dysfunction suspected
Administration of excessive hypotonic crystalloid or isotonic dextrose solutions can result in
Hypoosmolality, hyponatremia»_space; neurologica abnormalities / seizures
Marked hyperkalemia is particularly common in
rhabdomyelosis, hemolysis, tumor lysis
- muscle weakness
- cardiac arrhythmias
Major cardiac complications of AKI
Arrhythmias
Pericarditis
Pericardial effusion
Survivors of an episode of AKI requiring temporary dialysis are at high risk for
progressive CKD, and up to 10% may develop end-stage renal disease.
A spectrum of different pathophysiologic processes associated with abnormal kidney function and a progressive decline in glomerular filtration rate (GFR
CKD
Stages of CKD are stratified by
Estimated GFR
Degree of Albuminuria
Accumulation of toxins, fluid, and electrolytes normally excreted by the kidneys results in
Uremic Syndrome
Requires dialysis or kidney transplant
Most common inherited form of CKD
Autosomal Dominant Polycystic Kidney Disease
Clinical and laboratory complications in CKD become more prominent in what stages?
CKD Stage 3 and 4
Some of the most evident complications of CKD include
anemia and associated easy fatigability
decreased appetite with progressive malnutrition
abnormalities in calcium, phosphorus, and mineral-regulating hormones, such as D3 (calcitriol), parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF-23)
abnormalities in sodium, potassium, water, and acid-base homeostasis
Normal GFR in elderly
GFR values can be compatible with CKD stage 2 or 3, but most will show no further deterioration of kidney function
The most frequent cause of CKD in North America and Europe is
Diabetic nephropathy (mostly TIIDM)
When no overt evidence for a primary glomerular or tubulointerstitial kidney disease process is present, CKD is often attributed to
HTN
Major causes of CKD
- Diabetic nephropathy
- Glomerulonephritis
- Hypertension - associated CKD
(includes vascular and ischemic kidneydisease and primary glomerular disease with associated hypertension) - Autosomal Dominant Polycystic Kidney Disease
- Other cystic and tubulointerstitial nephropathy
Uremic syndrome can be divided into manifestations in three spheres of dysfunction
(1) those consequent to the accumulation of toxins that normally undergo renal excretion, including products of protein metabolism
(2) those consequent to the loss of other kidney functions, such as fluid and electrolyte homeostasis and hormone regulation
(3) progressive systemic inflammation and its vascular and nutritional consequences
GFR which is diagnostic of CKD
a GFR < 60, and/or presence of kidney damage (proteinuria) for > 3 months
Stage 1 CKD
Kidney damage with normal GFR >90
Persistant albuminuria
- Asymptomatic, SrCr/BUN normal,
- Acid-base compensated to normal (via increase in remaining nephron function)
Stage 2 CKD
Kidney damage with mild decrease in GFR, 60-89
- Asymptomatic, SrCr/BUN normal,
- Acid-base compensated to normal (via increase in remaining nephron function)
Stage 3 CKD
Moderate decrease in GFR, 30-59
- May still be symptomatic, but SrCr/BUN increase
- PTH, EPO, D3 become abnormal
Stage 4 CKD
Severe decrease in GFR 15-29
*Symptomatic - with anemia, acidosis, hyperkalemia, hypocalcemia, hyperphosphatemia
Stage 5 CKD
Kidney failure with GFR < 15
Seen almost exclusively in patients with CKD, livedo reticularis and advances to patches of ischemic necrosis, especially on the legs, thighs, abdomen, and breasts
Calciphylaxis
something to do w calcium imbalance and/or warfarin
Leading cause of morbidity and mortality in patients at all stages of CKD
Cardiovascular disease (10-200 fold increased risk of developing CVD if you have CKD)
- Ischemic CVD
- Cardiac troponin levels are frequently elevated in CKD without evidence of acute ischemia.
- HF
- HTN, LVH
HTN med of choose for CKD
ACE-I or ARB - esp w proteinuric patients
Comorbidity Tx goals in CKD
BP < 130/80
A1C 6.5 - 7.5%
LDL < 100
HDL > 50
Trigly < 150
Tobacco cessation
Weight los
Hemostasis Tx in CKD
EPO
Iron supps
Antiplatelet therapy
