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
Describe type 4 renal tubular acidosis, what abnormalities are noted (3)?
1) Deficit: hypoaldosteronism or renal resistance to aldosterone
2) Impact:
- Decrease Na absorption (distal tube)
- decreased H and K excretion (distal tube)
- hyperkalemia, acidic urine
- No stones
What is the major complication of ADPKD? What are some clinical features (5)? How is it diagnosed and treated?
1) 50% enter ESRD by 60s
2) Features: hematuria, abdo pain, HTN, palpable kidneys, intracerebral berry aneurysms, recurrent infection
3) Dx: U/S, CT, MRI
4) drain cysts if symptoatic, treat infections and HTN.
What are the clinical features of ARPKD (5)? How is it diagnosed? How is it treated/
1) Features: hepatic involvement (always), large size kidneys, HTN, pulmonary hypoplasia (neonate), oligohydramnios with Potter syndrome (neonate)
2) Dx: prenatal U/S
3) Tx: none. kidney transplant. Manage respiratory issues. Can be fatal in neonatal period.
What are the cause of renal artery stenosis (2)? What are the clinical features (3)? How is it diagnosed? How is it treated (3)?
1) Causes: atherosclerosis, fibromuscular dysplasia
2) Features: refractory HTN, low renal function, abdominal bruit
3) Dx: Imaging - renal arteriogram, MRA, contrast CT, Doppler U/S
4) Tx: renal angioplasty, bypass graft, conservative mgmt with meds (ACEi, CCB).
What are the types of renal stones, list in order of most to least common (4)?
1) Calcium stones
2) uric acid stones - precipitated in acidic urine, not seen on Xray
3) Struvite stone (staghorn) - associated with recurrent UTIs, precipitated by alkaline urine
4) Cystine stones - genetic predisposition (cystinuria)
- stones >1cm do not pass spontaneously
Discuss the indications for transrectal ultrasound (TRUS) with biopsy in prostate cancer work-up wrt PSA values and DRE findings.
1) If PSA > 4.0ng/ml, do TRUS with biopsy
2) If DRE abnormal, do TRUS with biopsy
How is prostate cancer treated in: localized disease, locally invasive disease, metastatic disease?
1) Localized disease - watchful waiting in elderly, otherwise radical prostatectomy (curative)
2) Locally Invasive - radiation plus androgen deprivation (not curative)
3) Metastatic - androgen reduction (orchiectomy, antiandrogens, LH, GnRH antagonists) (not curative)
What are the types of cells found in testicular cancers (4)?
1) Germ cell tumors (95%)
- Seminomas (35%) - highly treatable
- Nonseminomatous (65%) - embryonal carcinoma, choriocarcinoma, teratoma, yolk sac carcinoma
2) Non-Germ cell tumors (5%) - typ. benign
- Leydig cells
- Sertoli cells
What are the tumor markers in testicular cancer (2)?
- BHCG
- AFP
