CAM RENAL based of weaver slides

creatine

is from breakdown of muscle is suppose to be freedly filtered across the glomerulus and exreted in the urine

creatinine levels can be used to estimate

eGFR - takes into account gender, race, age

BUN

blood urea nitrogen

waste product of protein metab and filtred at the glomerulus, superior indicator of hydration

what can BUN be affected by

diet and elevated in UGIB (suuper gastrio intestional bleed)

azotemia

high creatine and BUN

uremia

renal impairment that results in build up of toxic waste products like DUN and creatine in the blood stream that causes sx

azotemia v uremia

azotemia is ealier on and is just the sx and uremia are the labs plus sx and indicate more progressed disease and tx is more intense like dialysis or transplant

what is tested in urine dipstick

• color and transparency

• pH

• specific gravity

• blood

• glucose

• ketones

• nitrites

• leukocyte esterase'

• bilirubin

• urobilinogen

• protein

does diptest actually test blood

no is test hemogloblin so can the falsley postive in rhabdo or other muscle disorders

functional proteinuria

benign and stems from acute illness and excerise will self reslolve

overload proteinuria

resorptive capicity of kidney is overloaded ex bence jones proteins

glomerular proteinuria

damage to the glomerulus increase permability

tubular proteinuria

faulty reabsorption

what are the causes or hematuria

1. renal causes:

   1. glomerular

   2. non glomerular

2. extrrarenal causes

   1. UTI, tumor, BPH, meds

hayline cast

can be seen n concentrated urine or after excerise

WBC cast

infection of inflammation so like pyelonephritis or intersitital nephritis

renal tubualr cell cast

ATN ot interstitial nephritis

muddy brown cast

ATN

RBC cast

glomerulonephritis

dysmphoric RBC in urine

common fiunding in glomerulnopheirits suggest glomerular source

criteria of AKI

• increase than 0.3 in baseline in 48 hrs or

• increase in creatine 1.5 in baseline in last seven days or

• urine less than 0.5mL/Kg/hr for six hours

aki manifestation

often asymptomatic presents with oliguria (less urine) more often than anuria (no urine)

associated labs with AKI

• matbolic acidosis

• hyperkalemia (peaked t waves, pr longer, QRS widen)

• hyperphosphatemia

what type of AKI will have bland sediment

prerenal and early post renal

AKI with high urine osmolality

points to prerenal

high urine Na in AKI

points to instrict (kidneys not doing their jobs)

BUN for prerenal

greater than 20:1

FENa less than 1

prerenal

FENa 2 or greater

intrarenal

FENa greater than 1

postrenal

what to order for post renal aki

untrasound od kidney and bladder and post viod residual

anticholingeric meds can cause

post renal AKI

what is the mc intrarenal aki

acute tubular necorosis

acute tubular necorsis

death of tubular cells in the kidneys

what kind of cast in ATN

muddy brown cast

causes of ATN

• ischemic: prolonged prerenal axotemia causes tubular damage

• nephrotoxic susbstances

what are the two types of nephrotoxic substances and what are examples

1. exogenous

   1. aminoglycosides, amphotericin B, NSAID, contrast dye, chemo

2. Endogenous

   1. uric acid (tumor lysis syndrome), rhabdo, bence jonce proteins (multiple myeloma)

ATN dx

BUN: CR less than 20: (intrarenal pattern)

FENa greater than 2 (intrarenal pattern)

urine microscopy of granular muddy brown cast

tx of ATLN

correct the underlaying cause

rhabdo

skeletal muscle necoris release creatine and myglobin and the myoglobin causes renal injury

what color urine in rhabdo

dark urine aka coke colored urine

tx of rhabdon

aggresive volume repletion with 0.9% normal saline

acute intersitiual nephritis

inflammatory or allergic response of renal interstitum with sparing of the gloneruli and blood vessels

mc cause of acute interstitial nephritis

drug hypersensitivity especually NSAIDS and abx

what is classic trais for intersitial nephritis

fever

maculopapular rash

arthralgias

microscopy of acute interstitial nephritis

WBC, and eosinophils

what are the causes of nephrotic syndrome

1. primary nephrotic syndrome

   1. minimal change disease

   2. membranous nephropathy

   3. focal segmental glomerulosclerosis

2. secondary nephrotic syndrome

   1. DM'

   2. SLE

   3. sarcoidosis

   4. infection, meds, malignancy

presentation of nephrotic syndrome

• edema

• frothy urine

• hypercoagulability (DVT/PE)

dx of nephrotic syndrome

heavy proteinuria and fatty cast (amltese cross shapes fat bodies)

gold standard= 24 urine with protein greater than 3.5

minimal change disease

destruciton of podocytes can occur after viral syndrome or be associated with allergeries or lymphoma

tx of minimal disease

steriods

minimal disease mc in

children (the mc nephrotic syndrome in children)

periorbital edema

minimal disease

focal segmental glomerulosclerosis

injusry of segmental glomerular scarring can be idopathic or from HTN and heronim, HIV

harder to filter due to the scarring

tx of focal segmental glomerulosclerosis

steriods if primary disease

membranous nephropathy

thickening of the glomerular basement membrane can be from autoantibodies or secondary from heptitis, SLE, penicillamine, breast lung and colon cancer

what would renal biopsy show for membranous nephropathy

subepitheliial immune complex deposits

membranous nephropathy tx

if primary steriods plus immunosupressants

what is a major risk factor for focal segment flomerulosclerosis

african descent

what population is membranous nephropathy mc in

caucasion men older than 40

clinical manifestation of nephritic syndrome

• coke colored urine

• hypertension

• oliguria less thajn 400 ml a day

nephritic syndrome is damage to the

glomerulus

causes of nephritc syndrome

• post infectious GN

• IgA nephropathy

• anti-GBM

• ANCA vasculities

• pulmonary renal syndrome

• membranoproliferative glomerulonephritis

what is another name for acute glomerulonephritis

nephritis syndrome

IgA nephoropathy (Berger disease)

occurs 24-48 hours after URI or GI infection is IgA immune complex deposits in the kidneys

what would you see in renal biopsy in IgA nephropathy

IgA mesangial deposits

tx of IgA nephritis

can self rewsolves

ACE for those with proteinuria

malatese cross shaped fat

nephrotic syndrome

post infectious glomerulnophritis

occurs after group strp A, impetigo, strep pharyngitis (10-14 days) but can occur with any infection caused from immune complex deposition in the glomerulus

dx of post infectious glomerulnophritis

positive ASO titers (antibodies against strep) low C3 and C4 levels

renal biopsy shows renal humps of IgM IgG and C3

tx of post infectious glomerulnonephritis

supportive care plus or minus antibotics

membranoproliferative glomerulonephritis

thickening og the basment due to immune complexes

membranoproliferative glomerulonephritis renal biopsy

tram tacking apperance

membranoproliferative glomerulonephritis tx

steriods

renal biopsy that shows immune humps of IgM and IgG with C3

post infectious glomerulnephritis r

renal biopsy that shows IgA mesangial deposits

IgA nephropathy

linear IgG deposits

anti GBM disease is a type of pulmonary renal syndrome so there are antibodies to the glomeruli and alveoli that causes pulmonary hemorrhage = hemoptysis

also known as goodpasture disease

anti GBM tx

plasmaphersis and immunosupressents

pauci immune necrotizingn crescentic glomerulnephritis

ANCA associated vaculitis to the small vessel vasculitis causes glomerlonephritis

RPGN rapidly progessive glomerulonephritis

clinical syndrome defined by rapid progression of GN mc from small vessel vasculities and anti GBM

criteria for CKD

progressive renal functional decline greater than 3 months

what are the most common and second mc cause of CKD

1= DM

2= HTN

what pathopys wise casues CKD

• mesengial hypertropohy

• podocyte effacement

• GBM thickening

• porximal epithelial cell damage

what stages of CKD are asymptomatic

1-4

uwhat does stage 5 manifest with

uremia

stage one of CKD

gfr 90 or above

stage 2 ckd

60-89

3a ckd

45-59

3bckd

30-44

4 ckd

15-29

5 ckd

less than 15 or on dialysis

presentation of uremia

accumulaion of waste cause metalic taste, puritis, pericarditis

BP goal to prevent CKD

less than 130/80

patient with risk factors should be monitored how frequently

every 3 yrs for albuminuria, decline gfr, and BP abnormailities

if GFR less than 30 what meds

thaized for early ckd ONCE BELOW 30 use loop diuretics

cardiovascular complications for CKD

• HF - use ACE and SGLT 2 I

• a fib

• pericarditis

vitamin D is needed for

intestines to absrobed less calcium

CKD and vit D

less vit D means less calcium means hyperparathyriodism and .increase in bone disease

renal osetodystrrophy

due to secondary hyperparathyriodism results in:

• osteitis fibrosa cystia: replacement of calcified bone with fibrious tissue

• osteomalacia= lack of bone mineralization and low vit D

brown boney tumors on fingers=

osteitis fibrosis cystica