nephrology Flashcards
RBC cast
diagnostic of glomerular bleeding. in acute or active glomerulonephritis
RBC morphology
blebs- gomerulus
biconcave- lower urinary tract
large # RBC
acute hemorrhage cystitis. bacterial/viral infection or chemo
hematuria
1) infection: UTI, hemorrhagic cystitis -adenovirus
2) trauma
3) hematologic: SCD, thrombocytopenia, thrombosis
4) metabolic: hypercalcemia
5) structural: tumor, obstruction, stone,
6) glomerular: berger’s, henoch schonlein purpura, post strep glomerulonephritis, alport’s sydnrome
proteinuria
> 100/d.
false pos if urine is very concentrated or on meds
TP/Cr is 2yo
urinary beta2 microglobulin
elevated in tubular proteinuria. freely filtered in glomerulus. usually completely reabsorbed at tubular epi. so if in urine, tubular injury
glomerulonephritis
inflm at glomeruli. usually immune mediated injury. primary- limited to kidney. secondary- part of a systemic disease (SLE)
P: variable. acute nephrite syndrome, nephrotic syndrme or asx
labs: urinalysis, urinary TP/Cr, blood chem, serm complemetn components, ab testing, IgA lvl.
types: poststrep GN, IgA nephropathy, Henoch schonlein purpura nephritis, membranoproliferative GN, SLE
acute nephrite syndrome
gross hematuria, HTN, signs of fluid overload from renal infuse
nephrotic syndrome
proteinuria, hyperchiilesteremia, edema
microalbumin
elevated in glomerular proteinuria. incr permeability
post streptococcal GN
dev 8-14d post infection of skin or pharynx or nephritogenic strain of GAS.
P: hematuria (gross), proteinuria, HTN+ fluid overload sx, low serum complement 3.
dx: ASO titer pos in 90% after pharyngitis. ABD titer pos after respiratory or skin infection with strep
tx: supportive. diet, ant-htn
IgA nephropathy
= merger’s disease. most common type of chronic GN.
etio: abn clearance of IgA complexes
P: repeat bouts of gross hematuria associated with respiratory infection. microscopic hematuria btw bouts
dx: renal bx-mesangial prolif and incr mesangial matrix
tx: supportive, ACEi, steroids
prog-variable
Henoch schonlein purpura nephritis
IgA mediated vascliits, nonthrombocytopenic palpable purpura on buttocks and thighs, abd pain, arthritis or arthralgia, gross or microscopic hematuria
membranoproliferative GN (MPGN)
lobular mesangial hypercellularity and thickening of glomerular GM.
nephritis or nephrotic syndrome + micro/gross hematuria, HTN, low serum complement, most pt dev end stage renal disease
tx: none, try corticosteroid, ace
nephrotic syndrome (NS)define and types
heavy proteinuria >50, hypoalbuminemia, hypercholesterolemia, edema
2/3 bf 5yo
3 categories
1) primary NS: 90% of all childhood cases. most common is minimal change disease (MCD)
2) NS from other primary glomerular disease like IgA nephropathy, MPGN, PSGN
3) NS from systemic disease like SLE
NS presentation
edema, follows URI. predispose to thrombosis 2/2 hypercoag –> renal vein thrombosis, DVT
incr rist for infection with encapsulated organism like strep pneumonia. present with spontaneous bacterial peritonitis, pneumonia or sepsis
NS dx
urinalysis 3+/4+ protien. CBC show elevated hct due to hsmoconc form hypoproteinemia. metabolic acidosis from renal tubular acidosis, hypoalbuuminemia elevated hl. C3, ANA antistrep ab to r/o other causes of NS. renal US-enlarge kidney. renal bx-rare
NS tx
dep on cause. supportive
hospitalized for initial tx
if widespread edema- IV infusion of 25% albumin
low salt diet, corticosteroid for MCD pt. empiric ab if febrile bc risk of pneumococcal infection
5% mortality from infection or thrombosis. response to steroid = less likely to dev ESRD
hemolytic uremic syndrome (HUS)
acute renal failure in presence of microangiopathic hemolytic anemia and thrombocytopenia
2 types: shiga toxin associated HUS and atypical HS
shiga toxin associated HUS (Stx HUS)
most common type in kids
e coli toxin
vascular endo injury by shiga toxin to end cells - plt thrombi formation and real ischemia
P: diarrheal prodrome (often bloody) then onset of hemolytic anemia, thrombocytopenia, acute renal failure
tx: supportive, no antibiotics. antibiotics for tx of coli in hemorrhagic colitis incr risk of HUS
prog- favorable, C- toxic megacolon
atypical HUS
drugs or inherited. P ~ Stx HUS although no diarrhea. supportive tx, stop meds, relapsing course. more become ESRD than sty HUS
hereditary renal disease
alport’s , multicystic renal dysplasia= most common cause of renal mass in newborn, ARPKD, ADPKD, medullary sponge kidney,
alport’s syndrome
progressive herediatary nephritis 2/2 side chain of type IV collagen in glomerular BM. x-linked dom.
HTN, hematuria, ESRD sometimes
hearing loss progressive, ocular abn in lens and retina
tx: tx HN with ACEi, renal transplant
ARPKD
uncommon. oligohydramnios, pul hypoplasia
greatly enlarge dcysic kidney. severe HTN, lier involved- cirrhosis, portal HTN
progressive - all need renal transplant
ADPKD
present 20-40yo. flank mass, UTI, hematuria, HTN, renal isuf. cerebral aneurysem.
need transplant
HTN et by age
neonates- most common cause- renal artery embolus after umbilical artery catheter placement, coarctation of aorta, congenital renal disease, renal stenosis
1-10yo: renal disease and coarctation
adolescents: renal disease and essential HTN
HTN features
infant: nonspecific. irritable, V, FTT, sz, CHF
kids: if acute malig HTN- HA, sz, stroke
kids with chronic HTN- growth retardation, poor school performance
renal tubular acidosis (RTA) define and types
inability of kidney to maintain normal acid base balance bc defect in bicarb conservation or excretion of H ions.
etio
1) congenital: mut in transporter of proximal or distal tubular cells
2) acquired: nephrotoxic drugs -amphotericin
RTA P by age
infant- growth failure and V
older kids- recurrent calculi, M weakness bone pain, myalgias
nephrocalcinosis-polyuria
hyperchloremic metabolic acids with normal serum anion gap!!
RTA eval
suspect in pt with non-anion gap hyperchloremic metabolic acidosis. confirm by venous blood gas.
calc urine anion gap= positive (Na+K-Cl).
eval for fanconi syndrome
acute renal failure
abrupt decr in ability to excrete nitrogenous wastes
P: lethargy, N/V, respiratory distress, HTN, sz, oliguria-nonoliguric
dx: lab: serum electrolyte, BUN, cr, UA, US, nuclar renal scan
tx: fluids. electrolyte, restrict protein intake, dialysis
chronic renal isuf and ESRD
most commonly glomerular disease.
prerenal failure
reversible decr in renal perfusion that leads to decr GFR. dehydration, hemorrhage, CHF, shock. incr bun/Cr>20. incr urine SG>1.03 osmolarlity>500 urine Na
renal parenchymal failure
damage to glomerulus (lupus, HUS,)- hematuria, proteinuria
damage to tubules (ischemic)- urinary Be micro globulin
interstitium (drugs)- eosinophilia, eosinophiluria, incr micro globulin
post renal failure
obstruction of urine flow by stones, tumor, ureterocele, trauma. dilation of renal collecting system on US
Vascular renal failure
decr perfusion of kidney due to renal artery embolus, renal vein thrombosis. decr blood on nuclear scan
dialysis
initiated if GFR is 5-10% of normal. peritoneal dialysis is preferred
multicystic dysplastic kidney
most common abd mass in newborn. associated with atrocity ureter
VUR
low dose prophylactic antibody to decr risk of UTI until outgrow VUR
urolithiasis
calcium salt. unusual in kid so look for predisposing metabolic D- hypercalciuria (idiopathic, fuosemid euse, familial hyeprcalciuria), hyperoxaluria (IBD), distal RTA, hyperuricouria, cystinuria, UTI, hyperPTH
labs: electrolyte, UA, BMP, PTH, uric acid lvl, venous blood gas to r/o RTA. urine testing, imaging-xray, stone fragment analysis
UTI
may present as enuresis in previously toleit trained
dx
1) neonate and infant: collect urine by suprapubic aspiration of bladder via sterile urethral catherization
2) leukocytes on microscopy>5-10. pos nitrite or luekocyte esterase
3) culture is gold standard
4) US and VCUG for all peel, recurrent UTI girls with cystitis
