Nephrology 2 Flashcards
What is urea osmotic diuresis?
Following AKI, high BUN leads to high urea in urea, which creates osmotic diuresis, leading to hypernatremia
preeclampsia clinical features
- new-onset HTN + proteinuria *occurs after 20 weeks of pregnancy
- new onset end-organ damage (liver, kidney, pulmonary edema, cerebral or visual symptoms, thrombocytopenia are also diagnostic)
What is eclampsia?
Presence of generalized tonic-clonic seizures in women with preeclampsia
anemia features in HELLP
Microangiopathic hemolytic anemia (thus, must have elevated bilirubin level and schistocytes on peripheral smear)
Composition of kidney stones in patient taking topamax
Calcium phosphate
Evidence for sodium bicarbonate in CKD
Thought to slow CKD progression and reduce mortality
When bicarb should be started in CKD
Serum bicarb chronically less than 22 (below reference range)
Most common reason for patients to have recurrent kidney stones
Hypercalciuria (not hypercalcemia), which is often idiopathic and commonly familial
Why thiazides are used to treat recurrent kidney stones
Thiazides cause calcium reabsorption, thus decreasing calcium content in urine
Milk alkali syndrome cause + clinical features
- ingestion of large amounts of calcium and absorbable alkali (eg calcium carbonate)
- hypercalcemia + metabolic alkalosis + AKI
When does pseudohyperkalemia occur?
Extremely high levels of leukocytes or platelets (caused by intracellular release of potassium by leukocytes in specimen)
Management of edema in nephrotic syndrome refractory to loop diuretic
- add thiazide (metolazone typically) and or potassium-sparing diuretic
Definition of high and low urine chloride
Low is less than 5
High is greater than 15
How albumin challenge works
- no improvement in creatinine with albumin administration suggests hepatorenal syndrome
Gestational hypertension vs chronic hypertension
chronic = hypertension starting before pregnancy or before 20 weeks of gestation (suggesting it preceded pregnancy) gestational = hypertension developing later on in pregnancy, after 20 weeks (blood pressure typically declines in first 2 trimesters and then rises in 3rd trimester)
Pathogen responsible for infection-related glomerulonephritis in which patient develops glomerulonephritis during infection
staph aureus
infection-related glomerulonephritis vs. post-streptococcal glomerulonephritis
infection-related glomerulonephritis = AKI in the setting of infection
post-streptococcal glomerulonephritis = Latent period between resolution of infection and acute onset of nephritic syndrome. pathogen is typically streptococcal
Pathogen responsible for most post streptococcal glomerulonephritis
Group A strep or strep pyogenes
What is monoclonal gammopathy of renal significance?
- patients who would otherwise be MGUS but have an abnormal UA and AKI
Management of patient with MGUS and AKI
Kidney biopsy for MGRS (demonstrating presence of monoclonal immunoglobulin deposition in the kidney)
tacrolimus mechanism of action
calcineurin inhibitor
Classic bone disease resulting from CKD or dialysis
Osteitis fibrosa cystica
Bone disease in CKD/ESRD patients but with normal labs –PTH/vitamin d/calcium
Adynamic bone disease
Osteitis fibrosa cystica pathophys and labs
- High PTH leads to increased bone turnover and alk phos levels
Term for mineral bone disease associated with vitamin D deficiency
osteomalacia
Most common cause of membranoproliferative glomerulonephritis
Hep C
what is the definition of hypertension per ACC/AHA guidelines?
SBP greater than 130 or DBP greater than 80 (SBP between 120-129 is defined as elevated blood pressure)
Kidney disorder in patients from balkans + clinical features
- Balkan endemic nephropathy
- urothelial cancers
Management of Balkan endemic nephropathy
cystoscopy + upper urinary tract imaging
goal percent sat in CKD
30%
Management of ACEi/ARBs when small bump in Creatinine
continue
GFR cutoff for SGLT2 inhibitors
GFR over 30
*continue if only small bump
Statins okay in CKD?
Continue statins in CKD
NEVER start when on dialysis (okay to continue)
Dysmorphic RBCs think
nephritic disease
know kimmelstein wilson nodule
see photo online
Which GN is associated with a resistance to African Sleeping Sickness?
FSGS (this is why it’s more common in blacks)
Only patient population in which FeNa is indicated?
Oliguric patients
Other causes of low FeNa
- contrast induced nephropathy
- rhabdo
- GN
Major SE of vaptans
- liver failure
management of renal stones greater than 10mm without clinical improvement
shock wave lithotripsy
Treatment of chronic kidney stones
- Decrease sodium intake
- normal to increased dietary calcium
IF urine citrate is low – potassium citrate
IF urine calcium high – thiazide
Ingredient in APAP that causes pyroglutamic acidosis
5-oxoproline
Type 1 vs type 2 RTA
Type 1 = stone forming
Type 2 = no stones
GFR cutoff for starting SGLT2
GFR greater than 30
calciphylaxis treatment
sodium thiosulfate
Sirolimus and everolimus mechanism
MTOR inhibitors
Clinical use of urine anion gap + interpretation generally
Differentiating non gap acidosis
Positive = distal RTA, chronic respiratory alkalosis
negative = diarrhea
drugs that are most common causes of AIN
antibiotics
*PPIs
NSAIDS
AIN clinical features + lab features
- rash, fever, eosinophilia
- pyuria, hematuria, *white blood cell casts, varying degrees of proteinuria
- may or may not have urinary eosinophils, not very useful
- patients rarely have all 3
Treatment of AIN
- discontinue offending drug
- systemic steroids
lab features of immune complex or post streptococcal GN
proteinuria + RBC casts
Interpretation of Weber test
IF sensorineural hearing loss –> lateralization to unaffected ear
IF conductive hearing loss –> lateralization to affected ear (ambient noise dampens sensitivity on unaffected side)
Management of acute sensorineural hearing loss
audiometry + MRI
Causes of conductive hearing loss
Any cause that limits sound from gaining access to the inner ear (otitis externa or *media, cholesteatoma, trauma, cerumen, *tympanic membrane perforation)
Management of moderate to severe exacerbation of COPD
Trial BPAP (unless contraindicated)
Other contraindications to BiPaP
- severe acidosis (pH less than 7.1)
- inability to clear secretions
- ARDS
- uncooperative or agitated
- upper airway obstruction
- facial surgery or trauma
Next step in young patient with pseudogout
Test for secondary cause (serum iron for hemochromatosis, hypothyroidism, hyperparathyroidism)
X-ray findings in pseudogout
- linear calcifications of menisci and articular cartilage
- chondrocalcinosis
Presentation of crystal-induced AKI
- acute flank pain + dysuria (presents similarly to nephrolithiasis but is bilateral) (drug precipitates in the tubules)
- AKI shortly after starting a drug
Treatment of crystal-induced AKI
- hydration
- alkalinize urine to pH greater than 7.15
- diuretic
- stop drug
Meds associated with crystal-induced AKI
- acyclovir
- sulfonamides
- MTX
- ethylene glycol
- protease inhibitors
- uric acid (TLS)
Diagnosis of crystal-induced AKI
- urine sediment analysis for crystals
Treatment of recurrent uric acid stones
Potassium citrate (which alkalinizes urine, and uric acid stones are highly soluble in alkaline urine) + hydration
Results of water deprivation test in primary polydypsia and nephrogenic and central DI
- water deprivation test = no change
- nephrogenic DI = no change
- central DI = increased urine osmolality
When eGFR is valid
- stable, steady-state clinical setting
- most accurate for CKD patients
*tend to underestimate actual
GFR
*less accurate for patients with a normal GFR and young patients
Management of abrupt onset severe psoriasis
test for HIV (common in patients with HIV infection and may be initial manifestation of disease)
Other factors that can precipitate psoriasis
- streptococcal infections (guttate psoriasis)
- smoking, drinking
- withdrawal from systemic steroids
association of explosive onset multiple itchy SKs
GI malignancy
association of recurrent herpes zoster
HIV infection
associations of multiple skin tags
- insulin resistance
- pregnancy
- Crohn’s
Management of suspected thoracic aortic dissection in patient with renal insufficiency
TEE
How to test for pseudohyperkalemia
redraw arterial blood with care to prevent hemolysis (no tourniquet or shaking, stored on ice, analyzed promptly)
Diagnosis of BK polyoma virus
- renal biopsy + IHC using antibodies against BK virus
specific finding of BK polyoma virus
Intranuclear inclusions
why are calcimemetics (cinacalcet) used to treat CKD patients with secondary hyperPTH and hyperphosphatemia?
- decrease frequency of fractures and reduce rate of parathyroidectomy
- also reduce cardiovascular disease in older patients
First step in management of hyperphosphatemia in CKD patients
reduce dietary phos
Second step in management of hyperphosphatemia in CKD patients
IF serum calcium low – calcium carbonate or acetate
IF serum calcium high – sevelamer
management of secondary hyperPTH in CKD patients
IF serum phos high – start cinacalcet
IF serum phos low – add vitamin D analog
MOA of calcimemetics
- increase calcium sensitivity of calcium-sensing receptors on PTH glands and reduce serum PTH, calcium and phos levels
Clinical features of ADPKD
- hepatic + pancreatic cysts
- cardiac valvular disease (mitral or aortic regurg)
- intracerebral aneurysms (may say family history of CVA)
- multiple unilateral or bilateral kidney cysts (can be asymptomatic otherwise)
Presentation of scurvy
alcoholic or malnourished patient with petechiae + bruising + bleeding gums and dental caries + impaired wound healing
treatment of scurvy
oral or injectable vitamin C
Luekocytoclastic vasculitis clinical features
petechiae and or palpable purpura 7-10 days after starting a new drug (eg penicillin) OR new infection
Definition of nephrotic range proteinuria
Greater than 3 g/24 hour period
orthostatic proteinuria clinical features
young adult + healthy otherwise + (generally less than 1 g/day but may surpass 3 g/day in select patients)
*proteinuria in the upright position but minimal to no proteinuria in the supine position.
When patients have transient proteinuria
Fever and after exercise
When dialysis access is needed
- typically when GFR is 15-20
- AV fistula’s are preemptive placed if hemodialysis is antiquated (maturation of a fistula takes up to 3 months)
- waiting until dialysis is emergently required places patients at high risk for complications
Correlation of uremia with bleeding risk in CKD
- no correlation with bleeding risk
Labs in uremic coagulopathy in CKD patients
- normal coags
- platelet count normal
- prolonged bleeding time
How does conjugated estrogen treat bleeding coagulopathy?
Thought to be from increased platelet reactivity
How does DDAVP treat bleeding coagulopathy?
- increases release of Factor VIII and von willebrand factor polymers from endothelial storage sites
Dysmorphic RBCS in the urine suggest what?
Glomerular disease
Presentation of IgA nephropathy
- one or more episodes of gross hematuria + typically following a URI
- proteinuria
- IgA immune complex
IgA nephropathy vs. Infectious GN in terms of physiology
IgA nephropathy = immune complex, IgA mediated (HSP is a subtype)
Infection-related GN = immune complex but not IgA
Next step after patient presenting with hematuria following URI
Quantify proteinuria
Relationship between creatinine and GFR and implication for interpreting Cr
- non-linear (exponential) - very time GFR halves, serum creatinine doubles
- so when GFR is normal, large decreases in GFR result in only small increases in creatinine
- and thus when GFR is significantly decreased, small decrements in GFR produce relatively large changes in serum creatinine
