Step Up - Renal Flashcards
Provide a framework for characterizing AKIs and provide the etiologies within each category (3).
1) Prerenal (40-80%)
a) Volume loss or sequestration
b) Low CO
c) Hypotension
2) Postrenal (5-15%)
a) Intrarenal - crystals, protein
b) Extrarenal - pelvis, ureter, bladder, urethra involvement
3) Renal (10-30%)
a) GN
b) Vascular disorder - small or large vessel
c) Interstitial disorder
d) Acute tubular necrosis
Why should NSAIDs and ACEi be avoided in patients with decreased renal perfusion (prerenal AKI)?
1) NSAIDs - constrict afferent arteriole
2) ACEi - efferent arteriole vasodilation
- both further reduce renal blood flow
- prerenal insult can become ATN if ischemia persists
With respect to prerenal AKI, comment on anticipated findings/values on urinalysis, BUN/Cr ratio, FeNa, Urine Osmo, Urine Sodium
1) Urinalysis - bland, hyaline casts
2) BUN/Cr - >20:1
3) FeNa less than 1%
4) Urine Osmo >500 mOsm
5) Urine Na less than 20
- adequate resorption
With respect to intrinsice AKI, comment on anticipated findings/values on urinalysis, BUN/Cr ratio, FeNa, Urine Osmo, Urine Sodium
1) Urinalysis - abnormal
2) BUN/Cr - less than 20:1
3) FeNa - 2-3%
4) Urine Osmo 250-300 mOsm
5) Urine Na >40
- impaired resorption
Describe the cells/casts seen in prerenal, intrarenal (ATN, GN, AIN), and postrenal urinalysis. Comment on the presence and amount of protein and blood seen.
1) Prerenal - benign U/A (few hyaline casts), no blood or protein
2) ATN - muddy brown casts, granular casts, trace protein, no blood
3) GN - RBC casts, fatty casts, 4+ protein, 3+ blood
4) AIN - WBC casts, eosinophils, 1+ protein, 2+ blood
5) Postrenal - Benign U/A, no blood or protein
What are the 3 most common causes of Chronic Kidney Disease?
1) DM
2) HTN
3) Chronic GN
- Any AKI can lead to CKD if prolonged or treatment not provided
Comment of the electrolyte disturbances and acid/base disturbance seen in Chronic Kidney Disease (K, Mg, Ca, Phos). Why does each one exist?
1) hyperkalemia - decreased urinary secretion
2) hypermagnesemia - decreased urinary loss
3) Hyperphosphatemia - decreased renal clearnace
4) Hypocalcemia - due to decrease vit D production. Leads to hyperparathyroidism and possible hypercalcemia and renal osteodystrophy
5) Metabolic Acidosis - due to decreased renal H clearance and ammonia production
What are the absolute indications for dialysis in ESRD (hint: AEIOU)?
A - acidosis (signnificant) E - Electrolytes (high K) I - Intoxicants (methynol, lithium) O - Overload (hypervolemia not managed otherwise) U - Uremia SSx (ex. pericarditis)
Define proteinuria. What are the features of nephrotic syndrome (5)?
1) Proteinuria - >150mg/day
2) Nephrotic syndrome
a) Urine protein > 3.5g/day
b) Hypoalbuminemia - increase loss, causes edema
c) Edema - caused by hypoalbuminemia and hyperaldosteronism
d) Hyperlipidemia - high synthesis of LDL and VLDL (due to liver albumin production rate)
e) Hypercoagulable state - loss of anticoagulants in urine
Contrast nephritic and nephrotic syndrome in terms of there presentations.
- both can be present in a GN
1) Nephritic - hematuria, azotemia, mild proteinuria, HTN, edema
2) Nephrotic - high proteinuria, hypoalbuminemia, hyperlipidemia, edema, hypercoagulable state and increased infection risk.
Briefly list and describe the primary glomerular disorders (GNs) (5).
- GN tx: steroids and cytotoxic agents
1) Minimal change disease - nephrotic syndrome, pediatric population, fusion of foot processes on EM.
2) Focal segmental glomerulosclerosis - poor prognosis, progressive
3) Membranous glomerulonephritis - Nephrotic syndrome, thick glomerular capillary walls, prognosis fair-good.
4) IgA nephropathy - hematuria, linked to URTI, IgA and C3 deposition on EM, prognosis good.
5) Hereditary nephritis - inheriteded disease with variable penetrance, no Tx.
Briefly discuss 3 secondary glomerular disorders (GNs)
1) Membranoproliferative - Infectious etiology (Hep C/B, syphilis, lupus). Poor prognosis
2) Poststreptococcal GN - nephritic syndrome, pediatric population, self-limited
3) Goodpasture Syndrome - IgG antiglomerular basement membrane antibody, biopsy shows linear immunofluorescence pattern, Tx: plasmapheresis
What are the causes of acute interstitial nephritis (4)? What are the clinical features (3)? How is it treated (3)?
1) Causes: allergic reaction to medication, infection, collagen vascular disease (sarcoidosis), autoimmune (SLE, sjogren)
2) Features: AKI, rash/fever/eosinophilia, pyuria/hematuria
3) Tx: stop offending agent, steroids, treat infection
Describe type 1 renal tubular acidosis, what abnormalities are noted (4)?
1) Deficit: inability to secrete H at the distal tubule
2) Impact:
- hypokalemia
- renal stone/nephrocalcinosis
- rickets/osteomalacia
- hypokalemic, hypercholermic nonanion gap metabolic acidosis
Describe type 2 renal tubular acidosis, what abnormalities are noted (3)?
1) Deficit: inability to resorb HCO3 at proximal tubule
2) Impact:
- loss of K and Na
- hypokalemic, hyperchloremic nonAG met. acidosis
- No stones