nephrology Flashcards
alternative marker for GFR thats not affected by age or muscle mass
serum cystatin c
what can cause an overestimation of GFR
falsely low Cr from loss of muscle mass because of advanced age, liver failure, or malnutrition
what is the only protein detected on a UA
albumin
what test thats not widely use can detect albumin with other proteins
sulfosalicylic acid (SSA) test
urine protein of >150 mg/g but <200 mg/g can indicate while protein >3500 indicates
tubulointerstitial disease or glomerular disease
vs glomerular disease
Proteinuria is a marker of and cand indicate
l parenchymal and glomerular disease and an independent predictor of progressive kidney disease,
cardiovascular disease, and peripheral vascular disease.
how to diagnose orthostatic/positional proteinuria
by obtaining split daytime
(standing) and nighttime (supine) urine collections.
coexisiting protein and hematuria can indicate what subtype of disease
glomerular causes of hematuria, even in the absence of casts.
Hematuria with preserved erythrocyte morphology in the urine, often without proteinuria or casts, is consistent with
extraglomerular bleeding (GU cancer, kidney stones, trauma, infection, and medications)
work up for hematuria
- urinalysis or urine culture to exclude infection, and if normal…
- noncontrast helical CT to detect calculi and contrast CT to detect renal cell carcinoma, and if normal…
• urine cytology, then stop evaluation if normal and patient is at low risk for malignancy (age <35 years, female sex, no other
risk factors), otherwise…
• cystoscopy for patients with positive urine cytology, aged >35 years, male, or if risk factors for malignancy are present
(cigarette smoking, analgesic abuse, benzene exposure, or voiding abnormalities)
leukocytes in urine indicate
glomerular or tubulointerstitial inflammation, infection, or an allergic reaction.
sterile pyuria (pyuria and a negative urine culture) suggests
Mycobacterium tuberculosis, interstitial cystitis, or
interstitial nephritis.
Eosinophiluria indicates
AIN, postinfectious GN, atheroembolic disease of the kidney, septic emboli, or small-vessel vasculitis but abscence doesn’t rule out any of these either
causes for for blood on dipstick urinalysis in the absence of intact erythrocytes on urine microscopy
dialysis and rhabdo
Urine lipids and fat are almost always associated with
heavy proteinuria or the nephrotic syndrome.
These may appear as free lipid droplets, round or oval fat bodies, or fatty casts.
what are kidney us used for
nephrolithiasis
• kidney size and cortical thickness (increased echogenicity implies parenchymal disease)
• renal cysts and tumors
• obstruction and hydronephrosis
• bladder size, postvoid residual, and the prostate in bladder outlet obstruction
what are kidney CT used for
nephrolithiasis (noncontrast abdominal helical CT)
• renal tumors and cysts (contrast abdominal CT)
• causes of unexplained urologic/nonglomerular hematuria (CT urography)
what are kidney MRI used for
- when radiocontrast agents must be avoided (risk of nephrogenic systemic fibrosis in patients with CKD)
- to characterize renal masses, cysts, and renal vein thrombosis
- to look for renal artery stenosis using MRA with gadolinium contrast
indications for kidney biopsy
glomerular hematuria
• severely increased albuminuria
• acute or CKD of unclear origin
• kidney transplant dysfunction
contraindications for kidney biopsy
bleeding diatheses, severe anemia, UTI, hydronephrosis, uncontrolled
hypertension, renal tumor, and atrophic kidneys.
hypertonic hyperosmolar causes of hyponatremia
- glucose (most common)
- BUN
- alcohols
- mannitol
- sorbitol
- glycine (bladder irrigation during urological procedures)
lab studies consistent with hypovolemic hypoosmolar hyponatremia
Spot urine sodium <20 mEq/L
BUN/creatinine >20:1
causes of hypovolemic hyponatremia
GI or kidney sodium losses, mineralocorticoid
insufficiency
hypervolemic hyponatremia lab findings
Spot urine sodium <20 mEq/L (HF and cirrhosis
in absence of diuretic therapy)
Spot urine sodium >20 mEq/L (acute and
chronic kidney failure)
causes of hypervolemic hyponatremia
HF, cirrhosis, kidney failure
euvolemic lab finding possibilities
Spot urine sodium >20 mEq/L
Urine osmolality usually >300 mOsm/L
vs
Urine osmolality 50 to 100 mOsm/L
euvolemic hyponatremia with spot sodium <20 and osm >300 causes
SIADH, hypothyroidism, adrenal insufficiency
(Addison disease), cerebral salt wasting syndrome
Euvolemia (normal volume)
euvolemic hyponatremia with spot sodium <20 and osm 50-100 causes
Compulsive water drinking
illness that cause siadh
malignancy (SCLC); intracranial pathology; and pulmonary diseases, especially those that increase
intrathoracic pressure and decrease venous return to the heart
MEDS that cause siadh
thiazides, SSRIs,
tricyclic antidepressants, narcotics, phenothiazines, and carbamazepine.
what can happen with overcorrecting hyponatremia
Central pontine myelinolysis (osmotic demyelination syndrome) may occur if hyponatremia is corrected too rapidly.
tx for siadh hyponatremia
1st water restriction
2nd option loop diuretic with salt
3rd Demeclocycline
causes of hypernatremia
inadequate access to water (older patients in nursing homes), a kidney concentrating defect (DI, most commonly caused by lithium),
and/or impaired pituitary secretion of ADH (e.g., sarcoidosis). Most commonly, hypernatremia results from loss of hypotonic
fluids (GI, kidney, skin) with inadequate water replacement
causes of hyperkalemia
• hyporeninemic hypoaldosteronism (Type 4 RTA; commonly seen among patients with diabetes)
• acute and chronic kidney failure
• low urine flow states
• medications (ACE inhibitors, ARBs, potassium-sparing diuretics, pentamidine, trimethoprim-sulfamethoxazole, and
cyclosporine)
• potassium shifts (rhabdomyolysis, hemolysis, hyperosmolality, insulin deficiency, β-adrenergic blockade, and metabolic
ekg changes in hyperkalemia
peaking of the T waves and shortening of the QT interval. As hyperkalemia progresses, the PR interval is prolonged, a loss of P waves occurs, and eventual widening of the QRS complexes is seen with a “sinewave” pattern that can precede asystole.
significant hyperkalemia but no ecg changes likely means
pseudohyperkalemia
what matters more of severity of hyperkalemia serum amount or ekg changes
ekg
If hypomagnesemia is suspected, look for
neuromuscular irritability, hypocalcemia, and hypokalemia
causes of hypomagnesemia
- GI losses (diarrhea, steatorrhea, intestinal bypass, pancreatitis)
- kidney losses (loop and thiazide diuretics, alcohol-induced)
- medictxations (cisplatin, aminoglycosides, amphotericin B, cyclosporine)
- hungry bone syndrome following parathyroidectomy
tx for magnesium deficiency
Administer oral slow-release magnesium and IV magnesium sulfate to achieve a serum magnesium level >1 mg/dL
anion gap equation
e anion gap = [Na+] − ([Cl–] + [HCO3–])
causes of high anion gap metabolic acidosis
DKA
• CKD
• lactic acidosis (usually because of tissue hypoperfusion)
• aspirin toxicity
• alcoholic ketoacidosis
• methanol and ethylene glycol poisoning (also typically associated with an osmolar gap)
cause of normal anion gap metabolic acidosis
• GI HCO3
– loss (diarrhea)
• kidney HCO3
– loss (ileal bladder, proximal RTA)
• reduced kidney H+ secretion (distal RTA, type IV RTA)
• Fanconi syndrome (phosphaturia, glucosuria, uricosuria, aminoaciduria)
• carbonic anhydrase inhibitor use (acetazolamide and topiramate)
Urine anion gap for normal AG metabolic acidosis to differentiate RTA from extrarenal losses ie diarrhea
extrarenal bicarb loss - a markedly negative (-20 to -25 mEq/L) UAG.
RTA type 1 (urine bicarb/cl is impaired) - UAG being markedly positive (20-40 mEq/L).
Type 1 RTA metabolic findings
Normal anion gap metabolic acidosis hypokalemia positive UAG, urine pH >5.5 (only in the setting of systemic acidosis) serum [HCO3] ≅ 10 mEq/L
Type 1 RTA associated findings
Nephrolithiasis and nephrocalcinosis, autoimmune disorders (SLE, Sjögren syndrome), amphotericin B use, urinary obstruction
Type 2 RTA metabolic findgs
Normal anion gap metabolic acidosis, normal or negative UAG, hypokalemia, urine pH <5.5, serum [HCO3] ≅ 16-18 mEq/L
Type 2 RTA associated findings
Glycosuria, phosphaturia, uricosuria,
aminoaciduria, and tubular proteinuria (Fanconi
syndrome)
Type 4 RTA metabolic findings
Normal anion gap metabolic acidosis,
hyperkalemia,
positive UAG,
urine pH <5.5
Type 4 RTA associated findings
Diabetes mellitus, urinary tract obstruction
treatment of Type 1 RTA
A, administration of bicarbonate
treatment for type 2 RTA
The addition of a thiazide diuretic may help by inducing volume depletion, lowering the GFR, and thereby decreasing the filtered load of bicarbonate.
treatment for type 4 RTA
a, which will treat the acid-base disturbance. These
patients, often with early CKD and diabetes, may develop severe hyperkalemia following treatment with ACE inhibitors or
ARBs.
how to treat etoh ketoacidosis
IV normal saline, glucose, and thiamine
• If (Δ anion gap/Δ [HCO3]) is <1, consider concurrent normal anion gap acidosis.
concurrent normal anion gap acidosis.
• If (Δ anion gap/Δ [HCO3]) is >2
concurrent metabolic alkalosis
what does it mean when you have an increased osmolar gap
gap> 10 can suggest alcohol poisoning
Ethanol is the most common cause of alcohol poisoning. Methanol, isopropyl alcohol, and ethylene glycol can also
increase the osmolal gap.
major findings in ethanol poisoning and tx
CNS depression, oliguria, flank pain and hematuria
No anion gap but increased osmolar gap
Tx- supportive
major findings in isopropyl alcohol and tx
CNS depression, ↑ Ketones
No anion gap but increased osmolar gap
Tx- supportive
major findings in methonol and tx
windshield wiper fluid
CNS depression, Vision loss
increased anion gap and osmolar gap
Tx- Fomepizole, Dialysis (severe) and Folic acid
major findings in ethylene glycol and tx
anti-freeze
-CNS depression, Acute kidney injury, Calcium oxalate crystals in the urine
increased anion gap and osmolar gap
Tx- Fomepizole, Dialysis (severe)
types of nephropathy
Focal segmental glomerulosclerosis
membranous
minimal change and DM
Focal segmental
glomerulosclerosis associations
Most common cause of nephrotic syndrome in blacks
“Collapsing” variety associated with HIV
Associated with morbid obesity
Membranous
glomerulopathy Associations
Most common cause of nephropathy in whites
Positive antibody against phospholipase A2 receptor
Secondary causes include: infection (hepatitis B and C, malaria,
syphilis); SLE; drugs (NSAIDs); cancer (solid tumors, lymphoma)
High propensity for thrombosis, especially renal vein
thrombosis
Minimal change
glomerulopathy
Most common cause of primary nephrotic syndrome in children
10% of nephrotic syndrome in adults
Diabetic
nephropathy
Most common secondary cause of the nephrotic syndrome and the most common overall cause in adults
Annual measurement of albumin-creatinine ratio measured beginning 5 years after diagnosis of type 1 diabetes and at time of diagnosis of type 2 diabetes
hallmark sign of nephritis
dysmorphic erythrocytes and erythrocyte casts
types Pauci-immune GN (necrotizing GN with few immune
deposits, normal complement)
Granulomatosis with polyangiitis
Microscopic polyangiitis
Eosinophilic granulomatosis with polyangiitis
type of gns with Immune complex deposition (low complement with
exception of IgA nephropathy)
IgA nephropathy
IgA vasculitis (Henoch-Schönlein purpura)
LN
Infection-related GN
Membranoproliferative GN
Cryoglobulinemia (see Monoclonal Gammopathies and Cryoglobulinemia)
what is anti–Glomerular Basement Membrane Antibody Disease and what is it if pulmonary capillaries are involved
autoimmune disease caused by antibodies directed against type IV collagen.
it causes pulmonary hemorrhage (Goodpasture syndrome).
lab and biopsy finding in anti-glomberular basement membrane antibody disease
normal complement levels and elevated levels of anti-GBM antibodies. Kidney biopsy shows proliferative GN
with linear deposition of immunoglobulin.
tx for anti–Glomerular Basement Membrane Antibody Disease
cyclophosphamide and glucocorticoids, combined with daily plasmapheresis.
granulomatosis with polyangiitis anca association
c-anca RP-3
MPA is associated with anca
p-anca mpo
labs and biopsy in pauci immune gn
Complement levels are normal. Kidney biopsy shows absent or minimal staining with immunoglobulin
tx for pauci immune gn (MPO, GPA)
glucocorticoids and cyclophosphamide (or rituximab) with or without plasmapheresis.
most common presentations of IGA nephropathy
asymptomatic microscopic hematuria (with or without proteinuria) or episodic gross hematuria
coincident with a URI (synpharyngitic nephritis).
compliment level and biopsy in iga nephropathy
Kidney biopsy shows glomerular IgA deposits on immunofluorescence. Complement levels are normal.
tx for iga nephropathy
benign course without treatment; patients with proteinuria and risk factors for progression may benefit from ACE inhibitors or ARBs
IgA vasculitis (HSP) diagnosis
Diagnosis is confirmed either by finding an IgA-dominant leukocytoclastic vasculitis or by kidney biopsy, which shows lesions
similar to IgA nephropathy. Complement levels are normal
labortory findings of LN
ANA and anti–double-stranded antibodies are positive, and C3 and C4 complement levels are depressed
tx for LN based on class
Class I and II (minimal or proliferative mesangial) lesions require no specific therapy.
- Classes III and IV (focal and diffuse glomerular lesions) are treated with high-dose glucocorticoids and either IV cyclophosphamide or mycophenolate mofetil.
- Class V (membranous) LN has a course similar to idiopathic membranous glomerulopathy
post-strep/staph GN occurs when
poststreptococcal GN typically occur after a latent period of 1 to 6 weeks
diagnosis of Post-infectious GN
Diagnosis is clinical in nephritic patients who have an ongoing or preceding infection. Complement levels are low
membranoproliferative GN is associated with which illness/demographic
children or young adults as proteinuria or the nephrotic syndrome. It is associated with
immune complex disease (SLE), infections (hepatitis C), and monoclonal gammopathy
Causes of Glomerular Diseases Associated with Low Complement Levels
- postinfectious GN (e.g., endocarditis, Group A streptococcal infection)
- SLE
- cryoglobulinemia
- membranoproliferative GN
- atheroembolic disease
diagnosis criteria for ADPKD
- ≥2 cysts (unilateral or bilateral) for ages 15 to 29 years
- ≥2 cysts in each kidney for ages 30 to 59 years
- ≥4 cysts in each kidney for ages >60 years
when do you gene analysis test for ADPKD
if imagining is equivical
symptoms of ADPKD
Hypertension is a common presentation. More than 50% of patients develop recurrent flank or back pain from kidney stones,
cyst rupture or hemorrhage, or infection.
urgent uro referral is needed for kidney stones in what settings
pyelonephritis or urosepsis • AKI • large stones requiring surgical removal • bilateral obstruction • obstruction of a solitary kidney
most severe extra renal complication of adpkd
ruptured aneurysm
treatment for adpkd
treat symptoms: HTN and pyelo/cyst infection
consider screening for aneurysm for people with adpkd esp if they have fam history
what is hereditary nephritis
rare end stage renal disease Xlinked also known as alport syndrome
symptoms of hereditary nephritis
sensorineural hearing loss and characteristic ocular findings such as lenticonus. Proteinuria, hypertension, and CKD usually develop over time.
Tx for hereditary nephritis
none, patients get end stage renal disease by teenage to 4th decade of life
Pre-renal AKI: BUN-Creatinine Urine Osmolality (mEq/L) Urine Sodium FENa Urinalysis and Microscopy Ratio
>20:1 >500 <20 <1% Specific gravity >1.020; normal or hyaline casts
ATN: BUN-Creatinine Urine Osmolality (mEq/L) Urine Sodium FENa Urinalysis and Microscopy Ratio
10:1 ~300 >40 >2% (can be low in contrast nephropathy) Specific gravity ~1.010; muddy brown casts and tubular epithelial cells
post renal BUN: creatinine ratio
20:1
