nephrology Flashcards
types of acute kidney injury
prerenal AKI
Intrinsic AKI
postrena AKI
falsely elevated BUN
drugs steroids
git / soft tissue bleeding
protein intake
low bun
malnutrition
liver ds
siadh
how is gfr measuresd
creatinine clearence sighlt overestimatesbecause it is secreated
inulin
if a person is anuric the rate of rise of creatinine will be
0.5-1 / day and also depends on muscle mass
causes of prerenal azotemia
hypovolemia hypotension drugs NSAIDS, ACE inhibitor CHF renal artery obstruction cirrhosis
parameters to find out cause of azotemia
FeNa
BUN /Cr Uosm Urine NA urinanalysis
change in parameters in prerenal azotemia
urinalysis Hyaline casts
Bun/Cr Ratio ⬆️
Fena ⬇️
urine osmolality >500mosmol
urine Sodium ⬇️
change in parameters in intrinsic kidney injury
urinalysis abnormal
Bun/Cr Ratio ⬇️
Fe Na ⬆️
urine osmolality ⬇️
urine Sodium ⬆️
diagnosis of hepatorenal syndrome
exclide renal failure first
no improvement after 1.5l of colloid
role of PG in kidney
dilates the renal afferent inhibits by NSAIDS
how do ACE inhibitor prevent renal failure
short term inc in bun/creatinine by dec in GFR
long term dec intraglomerular pressure
can there be renal failure with obstruction to 1 kidney
No
retroperitoneal fibrosis caused by drugs
bleomycin
methylsergide
methotrexate
MCC of neurogenic bladder
diabetes and multiple sclerosis
most common complication of oliguric phase
hypokalemia
ATN causes
ischemic
dec in blood flow to the kidney shock, sepsis,DIC #toxic Causes include antibiotics(aminoglycosides,vancomycin), radio contrast agents ,NSAIDs(especially in the setting of CHF), poisons, myoglobinuria(from muscle damage,rhabdomyolysis,strenuous exercise), hemoglobinuria(from hemolysis), chemotherapeutic drugs(cisplatin),and kappa and gamma lightchains produced in multiplemyeloma.
phases of ATN
oliguric phase
•Azotemia and uremia—average length10 to14days
•Urine output # •Diuretic phase
•Begins when urine output is>500mL/day
•High urine output due to the following:
fluid overload(excretion of retained salt,water,other solutes that were retained during oliguric phase);
osmotic diuresis due to retained solutes during oliguric phase;
tubular cell damage(delayed recovery of epithelial cell function relative to GFR)
treatment of ATN
general measures
no specific RX
1.hydration to prerenal component no effects of diuretics , mannitol, dopamine
2. intrinsic cause
supportive treatment
3. postrenal
stone removal catherisation
wht is azotemia and uremia
azotemia refers to the elevation of BUN.
# •uremia refers to the signs and symptoms associated with accumulation of nitrogenous wastes due to impaired renal function. It is difficult to predict when uremic symptoms will appear,but i trarely occurs unless theBUN is >60mg/dl.
how to differentiate between intrarenal causes of AKI
Acute tubular necrosis
Intrarenal
“Muddybrown”casts,renal tubularcells/ casts,granular casts
preotein trace
blood -ve
Dysmorphic RBCs,RBCs with casts,WBCs with casts,fatty casts
protein 4+
blood 3+
WBCs,WBCs with casts,eosinophils
protein 1+
blood 2+
causes of steven johnson syndrome
penicillin
sulfadrug
rifampin
quinolones
causes of allergic interstial nephritis
drugs ( most commonl
infection
autoimmune ds
characteristic finding of allergic interstitial nephritis
drug rash
fever
eosinophiluria
eosinophilia
best initial test for allergic interstitial nephritis
urinanalysis
best initial test to for rhabdomyolysis
urinary dip stick
+for blood
- for cells
other test are
CPK levels
why does chrons ds causes hyperoxaluria
because chrons ds decreases fat absorbtion
⬇️
fat binds with calcium which was to bind with oxalte
⬇️
this leads to increased absorbption of oxalate
⬇️
hyperoxaluria
pappilary necrosis diagnostic test
CT scan ill show “bumpy” contours in the renal pelvis where the papillae have sloughed off.
There is no specific therapy for papillary necrosis.
pt of sickle ds comes with sudden flank pain and history of NSAIDS use wht is diagnostis
pappillary necrosis
wht can u do prevent contrast induced nephropathy
hydration
bicarbonate
acetylcystine
cause of red cell casts
glomerulonephritis
granular casts
ATN
white cell casts
pyleonephritis
interstitial nephritis
waxy cast in urine
chronic kidney failure
gross painless hematuria is a sign of
bladder or kidney cancer untill proven otherwise
defination of hematuria
> 3erythrocytes / HPF
most sensitive test for microalbuminuria
radioimmunoassay
2 normal anion gap metabolic acidosis
RTA
diarrhoea
man comes with envelope shaped crystals in urine wht could be the most possible cause
ethylene glycol antifreeze
best initial test for ethylene glycol antifreeze suicide attempt
urinanalysis showing envelope shaped crystals in urine of oxalate
cause of elevated metabolic acidosis
LA MUD PIE (Mnemonic)
Lactate (sepsis, ischemia, etc.)
Aspirin
Methanol
Uremia
Diabetic ketoacidosis (DKA)—Beta hydroxybutyric acid (BHB) and acetoacetate, which are formed from fatty acids, are an alternate fuel source because the cells cannot absorb glucose because there is a deficiency of insulin
Paraldehyde, Propylene glycol
Isopropyl alcohol,
Ethylene glycol (antifreeze, low calcium)
analgesic nephropathy
This patient's abnormal urinalysis
painless hematuria.
sterile pyuria
white blood cell casts,
trace proteinuria
suggests a non-glomerular disorder affecting the
tubulointerstitium or lining of the urinary tract. Given his chronic low back pain treated
with over-the-counter analgesics, he likely has analgesic nephropathy.
Chronic analgesic use with 1 or more analgesics (eg, nonsteroidal anti-inflammatory drug
such as aspirin) can cause chronic kidney disease due to chronic tubulointerstitial
nephritis.
Patients are typically asymptomatic with an elevated creatinine found
incidentally. Patients can also develop painless and prominent hematuria due to
papillary ischemia from analgesic-induced vasoconstriction of medullary blood vessels
(vasa recta). Significant papillary necrosis and sloughing may cause renal colic.
most common cause of drug induced chronic renal failure
analgesic nephropathy
most common pathologies seen with analgesic nephropathy
tubulointerstitial nephritis
pappikary necrosis
urinalysis finding of intrinsic renal failure
Her serum BUN and Cr ratio is less than 20:1.
Other
findings that support this diagnosis are:
1. Urine osmolality of 300-350 mOsm/L (but never <300)
2. Urine Na of >20 mEq/L
3. FE-Na ->2%
urinalysis finding of prerenal azotemia
bun / cr <20:1
urinary Na <1%
urine Osm >500
features of crystal-induced acute kidney injury
Clinical features of crystal-induced acute kidney injury
Common causes • Acyclovir ♧♧♧♧ • Sulfonamides • Methotrexate • Ethylene glycol • Protease inhibitors • Clinical features Usually asymptomatic • Elevated creatinine within 1-7 days of starting drug • Urinalysis can show hematuria, pyuria & crystals presentation • t Risk with underlying volume depletion, chronic kidney disease • Treatment
Discontinue drug, volume repletion
• Concurrent volume repletion while giving drug can
prevent kidney injury
The patient’s presentation is most likely consistent with crystal-induced acute k
alport syndrome♧♧♧♧♧♧
familial disorder which usually presents in childhood as ▪recurrent gross hematuria and
▪proteinuria
.▪ Sensorineural deafness usually occurs.
▪Electron microscopy findings
include alternating areas of thinned and thickened capillary loops with splitting of the
glomerular basement membrane
Most common cause of nephrotic syndrome in children;
minimal change ds
lipoid nephrosis
minimal change ds
finding of minimal change ds
biopsy
EM
immunofloresence
biopsy Structurally normal glomeruli; positive fat stains in glomerulus and tubules
Negative IF
EM shows fusion of podocytes and no electron-dense deposits
Most common cause of nephrotic syndrome in adults
focal segmental glomerulosclerosis
finding of FOCAL SEGMENTAL GLOMERULOSCLEROSIS
Negative IF;
EM shows focal damage of VECs
biopsy ¿
Diffuse membranous glomerulopathy biopsy ,EM,IF finding
Diffuse thickening of membranes;
silver stains show “spike and dome” pattern beneath VECs (subepithelial deposits)
Subepithelial ICs with granular IF
type 1 MPGN
Subendothelial ICs with granular IF
; ICs activate the classical and alternative complement pathways;
EM shows tram tracks caused by splitting of the GBM by an ingrowth of mesangium
type 2 MPGN finding
Diffuse intramembranous deposits (“dense deposit disease”); EM shows tram tracks
dense deposit ds
type 2 MPGN
causes of minal change ds
T-cell cytokines cause the GBM to lose its negative charge; selective proteinuria (albumin not globulins)
Secondary causes: Hodgkin lymphoma
Often preceded by an upper respiratory infection or routine immunization Usually normotensive (90% of cases), unlike other types of nephrotic syndrom
cause of focal segmental glomerulosclerosis
primary or secondary disease
; secondary causes—
HIV (most common glomerular disease; mainly in young black males) and
intravenous heroin abuse
cause of diffuse membranous glomerulopathy
Primary and secondary types;
secondary causes:
Drugs: e.g., captopril, gold therapy
Infections: HBV, Plasmodium malariae, syphilis
Malignancy: carcinomas, Hodgkin lymphoma
Autoimmune disease: SLE (nephrotic presentation)
causes of nephrotic syndrome
Common causes of nephrotic syndrome in adults are
, ,
minimal change disease,
focal segmental glomerulosclerosis
membranous glomerulopathy
amyloidosis.
membranoproliferative glomerulonephritis type1 and type2
pathgnonomic finding of diabetic nephropathy
Hyalinosis that affects both afferent and efferent arterioles i
most common cause of AA and AL amyloidosis
Multiple myeloma is the most common cause of AL amyloidosis, and
rheumatoid arthritis is the most common cause of AA amyloidosis.
salicylate toxicity causes which acid base disturbance
acute salicylate toxicity leads to respiratory alkalosis by
stimulating the respiratory center in the medulla and causing tachypnea (with resultant
low PaC02 as the C02 is blown off)
. It then causes an* anion gap metabolic acidosis *by
uncoupling of oxidative phosphorylation in the mitochondria leading to anaerobic
metabolism (with resultant low HCO; from acid buildup).
The arterial blood gas (ABG) in salicylate toxicity is most likely to show a
▪ low PaC02 (due
to primary respiratory alkalosis and respiratory compensation for metabolic acidosis) and
▪low HCO; (due to primary metabolic acidosis and metabolic compensation for respiratory
alkalosis).
▪In addition, the arterial pH is usually in the normal range as the 2 primary acid-
base disturbances shift the pH in opposite directions. As a result, this patient’s ABG is
most likely to show a near-normal pH with mixed respiratory alkalosis and metabolic
acidosis▪
. The low HC03- in this answer choice suggests a metabolic acidosis. Based on
the corresponding formula for respiratory compensation (Winter’s formula), the
expected PaC02 = [1 .5 • HCO;) + 8 ± 2 = [1 .5 • 12] + 8 ± 2 = 26 ± 2 mm Hg. Because
the observed PaC02 (20 mm Hg) is lower than the expected value (26 ± 2 mm Hg), there
is a coexisting primary respiratory alkalosis. If the patient had a process causing only
metabolic acidosis (and appropriate respiratory compensation), a low HCO;, low PaC02 ,
and acidic pH (pH <7.35) would have been expected as the compensatory processes do
not perfectly correct the pH to normal.
appropriate compensation for metabolic acidosis
PaC02 = 1.5 (serum HCo3·) + 8 _+ 2
appropriate compensation for metabolic alkalosis
⬆️PaC02 by 0.7 mm Hg for every 1 mEq/L rise
in serum HC03.
appropriate compensation for acute respiratory acidosis
⬆️ Serum HCo3· by 1 mEq/L for every 10 mm Hg
rise in PaC02
appropriate compensation for acute respiratory alkalosis
⬇️ Serum HC03·by 2 mEq/L for every 10 mm Hg
decrease in PaC02
wht is asymptomatic bacteriuria
Asymptomatic bacteriuria
Definition
>:100,000 CFU/mL bacteria
Risk factors • Pre-gestational diabetes mellitus • History of urinary tract infection • Multiparity • Escherichia coli (most common)
Common pathogens
• Klebsiella
• Enterobacter
• Group B Streptococcus
• Cephalexin
First-line treatment
• Amoxicillin-clavulanate
• Nitrofurantoin
• Fosfomycin
most common type of genitourinary cancer
transistional bladder carcinoma
kehr sign
, irritation of the peritoneal lining of the right or left hemidiaphragm may cause
referred pain to the ipsilateral shoulder (Kehr sign) as sensory innervation to the
shoulder originates from the C3 tQ C5 spinal roots; these roots are also the origin of the
phrenic nerve innervating the diaphragm.
extraperitoneal bladder rupture presentation
extraperitoneal bladder injury (EPBI), which may consist of
either contusion or rupture of the neck, anterior wall, or anterolateral wall of the
bladder. In
the case of rupture, extravasation of urine into adjacent tissues causes
localized pain in the lower abdomen and pelvis. Pelvic fracture is almost always
present in EPBI, and sometimes a bony fragment can directly puncture and rupture the
bladder.
Gross hematuria is also usually present, and urinary retention (evidenced
by suprapubic fullness in this patient) may occur, especially in the case of injury to the
bladder neck.
intraperitoneal bladder rupture presentation
the setting of blunt abdominal trauma, spillage of blood, bowel contents, bile,
pancreatic secretions, or urine into the peritoneal cavity can cause acute chemical
peritonitis, which is evidenced by diffuse abdominal pain and guarding. The superior
and lateral surfaces of the bladder compose the dome of the bladder and are bordered
by the peritoneal cavity. Therefore, rupture of the dome of the bladder causes urine
to spill into the peritoneum, leading to peritonitis. Bladder rupture after blunt trauma is
due to a sudden increase in intravesical pressure and most likely occurs following a blow
to the lower abdomen when the bladder is full and distended.
In addition, irritation of the peritoneal lining of the right or left hemidiaphragm may cause
referred pain to the ipsilateral shoulder (Kehr sign) as sensory innervation to the
shoulder originates from the C3 tQ C5 spinal roots; these roots are also the origin of the
phrenic nerve innervating the diaphragm.
most common site of urethral injury
The bulbomembranous junction ie junction of the anterior and posterior urethra is the most common site of urethral injury.
cause of bleeding in chronic renal failure
platelet dysfunction due to uremic coagulopathy
platelets donot degranulate
uremic toxins cause platelet dysfunction but count is normal
most common cause of chronic renal
insufficiency/failure in children.
Posterior urethral valves
diagnostic modalities of vesicourethral reflux
The definitive diagnosis of VUR is made by contrast voiding cystourethrogram.
Renal ultrasound is performed to screen for hydronephrosis.
Recurrent and/or chronic
pyelonephritis can lead to blunting of calices (calyceal clubbing) and focal parenchymal
scarring.
Renal scintigraphy with dimercaptosuccinic acid is the preferred modality for
long-term evaluation for renal scarring. Renal function should be followed by serial
creatinine. Patients should be monitored closely for complications of chronic renal
insufficiency, such as hypertension and anemia.
acid base disturbance due to AKI
AKI can also cause an anion gap acidosis due to
retention of unmeasured uremic toxins which can also cause encephalopathy. However
the normal anion gap suggests that the elevated blood ure.a nitrogen can be due to other cause like
Gl bleed (ie, metabolism of blood proteins to urea) and there is not likely to be
an excessive concentration of other unmeasured uremic toxins.
and if thr pt has mental status
changes tht are therefore less likely to be due directly to her AKI.
most common cause of death in dialysis pt
CARDIOVASCULAR disease
most common cause of death in renal transplant pt
CARDIOVASCULAR disease
