Nephrology

 Abs in Goodpasture’s syndrome formed against  type IV collagen

 Loin to groin pain + hx of passing sand  calcium oxalate

 HTN, you gave ACE, what to add  amlodipine

 ICU in shock, phosphate decreased, organ damaged is  kidney

 Difficulty initiating urine, distended bladder and large prostate in 80y.o  BPH  SAME
SCENARIO, type of incontinence  overflow

 Bilateral abdominal mass + undergo dialysis in 20y.o man  PCKD

 Ureteral stones not visible on xray  uric acid

 Measure to reduce UTI recurrence  vaginal probiotics

 Renal artery stenosis on renography, next step  CT angiography

 60y.o + long hx of uncontrolled HTN + headache and bp 160/90, what will u see in
kidney  increase hyalinization of arterioles

 Back pain, dysuria, frequency in 80y.o  PSA is next

 Most common cause of renal failure  DM

 Abnormality in Fanconi syndrome  metabolic acidosis

 Child with tea urine and swelling, next  urnialysis

 DM + prevent progression of renal disease  ACEI

 RISK FACTOR for pyelonephritis  spermicide use

 Most common mode of inheritance in PCKD  autosomal dominant

 Gold standard to measure GFR  inulin excretion

 Key feature in nephritic syndrome  HTN

 18Y.O male + bilateral flank pain for 6m + mutation in ch16  autosomal dominant
PCKD

 40y.o male + RIGHT flank pain, no dysuria of sicharge  nephrolithiasis! “pain is uni, no
signs of infection”
 Most common GM  IgA nephropathy!

 Edema + proteinuria  nephrotic syndrome

 80y.o + acute urine retention  foley cath & urine culture

 On diuretics for HTN + muscle weakness, irritability, diarrhea  hyperkalemia

 Bad prognosis in HSP  renal failure

 20y.o + soda urine for 4d + congestion of throat, cervical lymph, and fever  IgA
nephropathy “post-strepto occur 2-5w after”

 BPH sx, rx  Tamsulosin “alpha adrenergic blocker”

 Patient swallowed 1l of anti-freeze  acute tubular necrosis “ethylene glycol”

 Beads on a string  fibromuscular dysplasia

 Patient with one kidney larger than the other (14 & 7 cm) next  CT angio

 DM + present with dyspnea, pallor, edema and itching  renal failure

 Most common sign of renal cancer  hematuria

 Hemoptysis, and nephropathy + anti-GBM  goodpasture

 Aminoglycosides  acute tubular necrosis

 Screening for renal impairment in DM  albumin:creatinine ratio

 Histo findings in minimal change nephrotic syndrome  effaced podocytes

 Most common primary cause of nephrotic syndrome in ADULTS  focal segmental

glomerusclerosis

 Anti-basement abs  goodpasture syndrome

 Rx of hemolytic uremic syndrome  supportive therapy

 8y.o with nephrotic syndrome  oral prednisolone

 40y.o, smoky brown urine, pitting edema, urinalysis= 1+ protein, and 3+ rbc 
NEPHRITIC

 Suggestive of post-streptococcal GM  low serum c3 level

 Tubule with columnar cells on renal biopsy  collecting tubules

 Peak age for minimal change  3-6y

 1st line HUS  support, 1st line nephrotic  steroid

 Not a sx of BPH  (frequency, incontinence, dribbling, hematuria)

 Mechanism of diabetic nephropathy in early stages  sclerosis of arterioles and

increase in filtration rate**

 Ass/ with renal cell carcinoma  (VHL, sickle cell, renal dialysis, all)

 Goodpasture’s syndrome rx  plasmapheresis, cyclophasmaphide, and prednisolone

 Hematuria and calf muscle pain  rhabdomyolysis

 Minimal change  light microscopy= normal electron= fusion of podocyte

 Post-streptococcal GM rx  DIURETICS FOR EDEMA

 US showed bilateral hydronephrosis  PCKD

 Hematuria and proteinuria, had URTI 2w ago  diffuse proliferative GM

 Bilateral knee pain, palpable purpuric rash over butt and shins  NSAIDs “HSP”

 A STRONG support for GM dx  dysmorphic rbc in urine

 20y.o + CT= bilateral thin parenchyma of kidneys  PCKD**

 Sickle cell + painless hematuria, flank pain, fever, wt loss and fatigue, palpable mass in
abdomen!!!!!  renal cell cancer

 Smoker + hematuria + wt loss and loin pain, most common gene mutation  VHL

 ADH work on  collecting duct

 Controlled DM, and HTN on ACEi, furosemide, spironolactone, electrolyte normal 

stop spironolactone “ACE can cause hyperkalemia”

 Amino acids are completely reabsorbed via active transport in which part  proximal
convoluted tubules

 Peak of minimal change  2y

 Anion gap  Na – (HCO3 + Cl)

 Oliguria + peripheral edema over weeks + urinalysis show hematuria, proteinuria, and
dry cough, rbc cast in urine, biopsy= glomerular crescents  anti-GBM disease “rapidly
progressive GM= goodpasture, SLE, granulomatosis”

 Bladder cancer, gi system  bilateral hydronephrosis

 Patient on NSAIDS and many other  interstitial nephritis 2ndry to anti-inflammatory

medication

 Proteinuria and hematuria + mesangial expansion with increase in cells and matrix in
biopsy, in em= mesangial deposits  IgA GM

 One day after A RACEEEE + dark urine, urinalysis NEGATIVEEE for blood 
rhabdomyolysis

 HIV  FSGM

 Most common type of nephrolithiasis  ca oxalate

 Decreased urine output, hemoptysis  goodpasture’s, self-limited

 BPH + nausea and vomiting + Na= 145, BUN= 45, serum creatinine=2, urine Na= 10,
urine creatinine= 80  prerenal failure “high creatinine and bun indicate post, (10/145)
/ (80/2) * 100 = 0.17% “<1% prerenal”

 All can cause ARF except  “rhabdo, NSAIDS, ethylene, penicillin, iron”
 Chronic renal dialysis brought to ED in cardiac arrest  hyperkalemia
 Most common neurologic complication of chronic renal failure  encephalopathy
 HTN + calcium oxalate  hydrochlorothiazide
 Tenderness in renal angle and hematuria  KUB
 Initial pheochromocytoma  a-antagonist
 Most common electrolyte abnormality in advanced CRF  hyperkalemia
 Nephritic syndrome  HTN
 Mutated in PCKD  16ch
 New
 Difficulty initiating urine  overflow incontinence

 Radio-lucent stone on x-ray  uric acid “RU, UR”

 Most common cause of CKD  HTN “other choice was DI!”

 PCKD  autosomal recessive “dominant if in answers”

 Bilateral flank pain, ch16  autosomal dominant PCKD

 Prolonged vomiting  met alkalosis

 1st sx of hypo mg  muscle spasm

 Cells form filtration in kidney  podocyte

 HF & hyponatremia, 3+ pitting edema, bilateral effusion, best way to manage

hyponatremia  furosemide

 Cola urine, erythema of post pharynx and cervical lymphadenopathy and fever now 
IgA nephropathy**

 Anti-freeze  ATN

 Initial urge  bladder training & physiotherapy

 Urinary incon & palpable bladder  overflow incon

 Dyspnea & pallor & pedal edema & itching  CKD**

 Most common sign bladder ca  painless hematuria

 Middle age female, filling defect in right ureteropelvic junction with acoustic shadow, US
 kidney stone

 Best confirmatory for renal cell ca  partial nephrectomy**

 Recurrent UTI & large, bilateral kidney stones  proteus

 Anti-HTN, muscle weakness, diarrhea, irritability, electrolyte imbalance 

hypercalcemia

 pH 7.5, HCO 17, CO2 22  resp alkalosis

 pH 7.48, HCO 32, CO2 45  metabolic alkalosis

 sepsis & UTI, if he developed acute kidney injury, when earliest time cr will rise  48h

 sepsis & UTI, FeNa <1%  pre-renal

 muddy cast  ATN

 RBC  GN

 WBC  acute interstitial nephritis

 Multiple months of painless hematuria, suprapubic pain and inability to void for past
36h, cr 1.5  post-renal

 Multiple HTN med, presents with difficulty hearing and mild hypo k  stop furosemide

 Multiple HTN med, presents with hyperglycemia, hyperlipidemia, hyponatremia/mild 

stop thiazide