4 CKD And Nephrotic Syndrome Flashcards
What is the most common comorbid condition with CKD?
Diabetes
Continues to be the leading cause of ESRD
Gender difference in CKD prevalence
Women more commonly affected (18% vs 13%) but men tend to have more progressive course
What is the definition of CKD?
Decreased kidney function or kidney damage for 3 or more months
Glomerular filtration rate (GFR) < 60 mL/min/1.73m2
Evidence of kidney damage:
• Albuminuria*** Urine albumin:Cr ratio of ≥30 mg/g
• Abnormal imaging tests (U/S)
• Abnormal urinary sediment (ie RBC casts)
• Hx of kidney transplant
What is the best marker of kidney function?
GFR - declining GFR is the hallmark of progressive kidney disease
Serum creatinine is a poor measure of kidney function
Name the CKD Stage:
Kidney damage with normal or increased GFR (≥ 90)
Stage 1
Name the CKD Stage:
Kidney damage with mildly decreased GFR (60-89)
Stage 2
Name the CKD Stage:
Mildly-moderately decreased GFR (45-59)
Stage 3a
Name the CKD Stage:
Moderately-severely decreased GFR (30-44)
Stage 3b
Name the CKD Stage:
Severely decreased GFR (15-29)
Stage 4
Name the CKD Stage:
Kidney failure, GFR < 15
Stage 5 - add D if treated by dialysis
Name the Albuminuria classification:
ACR < 30 mg/g
Protein dipstick - negative to trace
Stage A1
Normal to mildly increased
Name the Albuminuria classification:
ACR 30-300 mg/g
Protein dipstick trace to 1+
Stage A2
Moderately increased
Name the Albuminuria classification:
ACR > 300mg/g
Protein dipstick >1+
Stage A3
Severely increased
What is important to know about measuring Albuminuria?
Must be verified by a repeated test - it has to be PERSISTENT over several months
What is the pathogenesis of CKD?
Progressive decline in the GFR typically over months to years, due to the IRREVERSIBLE DESTRUCTION OF NEPHRONS INDEPENDENT of the cause (still need to ID the cause though)
Destruction of nephrons leads to COMPENSATORY HYPERTROPHY and supranormal GFR of the remaining nephrons
Compensatory hyperfiltration leads to OVERWORK INJURY in the remaining nephrons
Progressive GLOMERULAR SCLEROSIS and INTERSTITIAL FIBROSIS
Because of the progressive nephron and GFR loss, what will you see in lab results?
Abnormalities in water, electrolyte, and pH balance
Accumulation of waste products normally excreted
Abnormalities in the production and metabolism of certain hormones (EPO, calcitriol)
What are the most common causes of CKD?
DIABETES
HTN
Glomerular disease
Polycystic kidney disease
Chronic Tubulointerstitial disorders
How should you screen patients at risk for developing CKD?
Urine albumin-to-creatinine ratio
Serum creatinine to estimate GFR (eGFR)
Who IS at risk for CKD?
60 years or older Diabetes HTN CVD FHx of kidney disease Ethnic minority Cancer Systemic infection (HIV or Hep C) Recurrent UTIs Nephrolithiasis Nephrotoxic drug exposure Autoimmune disorders Hx of AKI
What is the clinical presentation of CKD?
Dependent on underlying cause and stage
Sx develop slowly with the progressive decline in GFR
Asymptomatic in early stages
Sx may not manifest until kidney failure is far advanced
Nonspecific Sx - fatigue, for example - worry about uremic syndrome
Accumulation of metabolic waste products, or uremic toxins
Uremic syndrome
Often seen with a profound decrease in GFR (10-15 mL/min/1.73m2)
What are the SSx of uremic syndrome?
FATIGUE, MALAISE, anorexia, N/V
Pruritis, easy bruisability
Metallic taste in mouth
Shortness of breath
Dyspnea on exertion, PERICARDITIS
Restless legs, seizures, ENCEPHALOPATHY
What finding on renal U/S supports a diagnosis of CKD?
Small kidneys BL (<9-10cm) - decline in renal mass/atrophy
Although normal or enlarged kidneys may be seen as well
_________ may lead to death before the progression to ESRD
Complications of CKD
More likely to occur at later stages - why you need to ID complications early
May arise from the adverse effects of interventions used to prevent or treat
What are the main complications of CKD?
CARDIOVASCULAR DISEASE - a leading cause of death
HTN
Dyslipidemia
Anemia (b/c kidneys —> EPO)
Mineral/bone disorders
Fluid and electrolyte abnormalities (hyperkalemia, hyperphosphatemia, hypocalcemia, metabolic acidosis)
Uremia
Malnutrition (low serum albumin)
Spectrum of bone disorders that are a complication of CKD
Osteitis fibrosa cystica, adynamic bone disease, osteomalacia (bone remodeling and demineralization)
Typical pattern: hyperphosphatemia, hypocalcemia, decreased vitamin D, SECONDARY HYPERPARATHYROIDISM
CKD Mineral and Bone Disorder is often clinically detectable starting at what stage?
Stage 3 CKD
What are the keys to managing CKD?
IDENTIFY THE CAUSE
Identify and treat potentially reversible factors
Manage complications
Frequent review of meds (avoid nephrotoxic drugs, adjust drug doses when appropriate)
Identify and adequately prepare the patient in whom renal replacement therapy will be required
Reversible causes of kidney injury
Infection (do a urine culture/sensitivity)
Obstruction*** (bladder cath, renal US)
Volume depletion (BP, pulse, orthostatic measurements)
Nephrotoxic agents (drug history, recent imaging)
Heart failure (phys exam, CXR)
How do you slow the progression of CKD?
TREATMENT OF THE UNDERLYING CAUSE OF CKD
Glycemic control
BP control - ACE/ARBS to reduce proteinuria, low sodium diet
Weight management
Management of CV risk factors (statins, smoking cessation)
Why are ACE/ARBs so great for CKD patients?
RENOPROTECTIVE
Helpful in SLOWING THE PROGRESSION OF PROTEINURIC CKD (lowers albuminuria) in chronic stable patients
Inhibiting Ang II —> DILATES the EFFERENT arteriole —> reducing glomerular pressure
When are ACE/ARBs HARMFUL for CKD patients?
May see an acute reduction in GFR and hyperkalemia - ok in chronic states but a problem in acute settings
Use with caution in AKI
Contraindicated in bilateral renal artery stenosis***