Nephrology Flashcards
Nephrotic vs. Nephritis
NephrOtic:
- proteinuria ( > 3.5)
- edema
- hypoalbuminemia
- Oval fatty bodies ( maltase Cross) in urinalysis
- biopsy shows hypo-cellular specimen
- related to obesity—> hyperlipidemia+ edema + fatty casts/oval fatty body
NephrItic:
- proteinuria (< 3.5)
- hematuria
- HTN
Nephrotic syndrome primary etiology
- minimal change disease
- most common in children
- loss of negative charge in basement membrane promoting proteinuria (lack of charge at basement membrane) - Membranous nephropathy:
- Men > 40
- Malaria
- Medication (penicillinase) - Focal Segmental Glomerulosclerosis:
- seen with: HIV, heroin users, HTN
- most common in African American
Nephritic syndrome/ glomerulonephritis
1.IgA Nephropathy
- most common cause of acute glomerulonephritis
- most common affect young males
- occurs 24-48 hours after URI or GI infection
- Post infectious/ Post streptococcal Glomerulonephritis:
- most common after group A strep (GAS) infection
- Coca-Cola color urine
- seen in adolescent boy 2-14 years
- facial edema is common - GoodPasture’s Disease:
- Glumeronephritis + Hemoptysis
- anti-GBM antibody against the type 4 collagen of the glomerular basement membrane
Acute kidney injury —> Prerenal
- kidney is fine
- but decrease renal perfusion
- due to hypovolemia (volume depleted)—> ( diuretics, diarrhea, vomiting, dehydrated)
- other causes:
1. NSAIDS: Afferent arterial constriction
2. ACE-inhibitors: Efferent arterial dilation
Diagnosis:
- BUN/Cr ratio > 20:1
- Fractional excretion of sodium < 1%
- concentrated urine
- decrease urinary sodium < 20 (kidney are working fine, and able to retain sodium)
Treatment:
- IV fluid ( respond well !!)
Acute kidney injury —> Post-renal Azotemia
- due to obstruction (stop urine flow from kidney to bladder)—> (kidney stone, tumors, BPH, prostate, cancer)
Diagnosis:
- ultrasound —> look for sign of obstruction
Treatment:
- remove obstruction —> lithotripsy, urinary stent
Intra-renal or Intrinsic Renal Failure ( acute interstitial Nephritis, acute tubular necrosis)
- Acute Interstitial Nephritis:
caused by:
1. Medication (70%) —> NSAIDS, penicillin, Sulfa-, rifampin
2. infection, autoimmune process
clinical:
- fever, esosinophellia, rash
diagnosis:
- WBC casts ( neutrophils) seen in urinalysis
Treatment:
- remove offending agent
- Acute Tubular Necrosis:
- most common type of Intrinsic kidney injury
Caused by:
- ischemia —> prolonged prerenal azotemia
- nephrotoxic agents —> contrast dye, aminoglycosides
Diagnosis:
- Granular or muddy brown casts in urinalysis
- increase urinary sodium > 40 (kidney not working properly, unable to retain sodium)
- BUN/Cr ratio 10-15:1
Treatment:
- remove offending agent & IV fluid
Microscopic finding on Urinalysis
- Acute Glomerulonephritis or vasculitis:
- RBC Casts - Acute interstitial Nephritis or pyelonephritis:
- WBC casts - Nephrotic syndrome: ( or pre-renal azotemia)
- fatty casts or oval fat bodies - End stage renal disease:
- waxy casts
- or broad cast ( in CKD) - Interstitial nephritis
- Eosinophils - Acute Tubular necrosis (ATN)
- Muddy Brown Cast
- following a hypovolemic shock (prolonged hypotension)
- BUN/Cr ratio ( 10-15: 1)
- urine osmolality of 300-350 ( never < 300)
- urine Na > 20
- fraction excretion of Na > 2 %
Horseshoe kidney
- fusion at lower lobe of each kidney
- associated with:
1. Uritopelvic junction obstruction
2. Turner syndrome - increase risk for:
1. Pyelonephritis ( due to urinary stasis)
2. Kidney stone
3. Renal malignancy
4. Renal cell carcinoma
Clinical:
-most patients asymptomatic
Diagnosis:
- CT urography
Treatment:
- most cases require no treatment
Polycystic kidney disease
- autosomal dominant
- cyst is seen in the kidney or liver
Clinical:
- abdominal & flank pain
- increase risk for cerebral (berry) aneurysm & Mitral valve prolapse
PE:
- palpable flank mass
- HTN
Diagnosis:
- renal US
Treatment:
- increase fluid intake
- ACE-I/ARB
Chronic kidney disease (CKD)
-progressive functional decline for 3 months or more, accompanied by: proteinuria, abnormal urine, sediment, abnormal imaging
Stages of CKD:
1. Stage 1:
- GFR (>90) & proteinuria & abnormal urinalysis
- Stage 2:
- GFR (60-89) & proteinuria & abnormal urinalysis - Stage 3
- GFR (30-59) & proteinuria & abnormal urinalysis - Stage4
- GFR (15-29) & proteinuria & abnormal urinalysis - Stage 5:
- GFR (<15) indicates END stage Renal disease —> REQUIRE Dialysis
Causes:
1. Diabetic mellitus (1st)
2. HTN (2nd)
Diagnosis:
- proteinuria (24 hr urine, or albumin/Cr ratio)
- waxy cast (in urinalysis)
- renal US ( shows small kidney)
Treatment:
- treat HTN —> maintain BP < 140/90
- ACE-I or ARB in most patients
- A1C < 7
- dialysis at stage 5
Wilms tumor (Nephroblastoma)
- most commonly seen with children less than 5
Clinical:
- iris malformation ( aniridia = absence of iris)
- locked In position tumor (doesn’t cross midline of abdomen, unlike neuroblastoma of adrenal which does)
- mental retardation
- sexual malformation (hypospadias, cryptorchidism)
- palpable abdominal mass
- hematuria
- constipation
Diagnosis:
- abdominal US
Treatment:
- total nephrectomy with chemo 80-90% cure rate
Renal cell carcinoma (RCC)
- Tumor of the proximal convoluted renal tubule cells
- 95% of tumor in kidney
Risk:
- smoking, HTN, obesity, dialysis, Men
Clinical:
- Triad: hematuria + flank/abdominal pain + palpable abdominal mass
- left sided varicocele (due to the tumor blocking the left testicular vein)
- most common area of matastesis is the lung
Diagnosis:
- hypercalcemia ( tumor secrets PTHrP, which mimics primary hyperparathyroidism
- CT
Treatment:
- radical nephrectomy
Acid based disorder
Hepatorenal syndrome (HRS)
Seen in:
- seen with patients with liver cirrhosis secondary to systemic or renal hypoperfusion
- creatinine > 1.5
- urine sodium < 10
- absent of blood, protein, casts in urine
- renal function does not improve with IV fluid resuscitation
Caused by:
- splanchnic arterial dilation
Factors:
- reduce renal perfusion
- GI bleed, vomiting, sepsis, excessive diuretic use, SBP
- reduce glomerular pressure & GFR ( NSAIDs use—> constrict afferent arterioles)
Diagnosis:
- Fraction excretion of sodium < 1 % ( urine Na < 10)
- absence of tubular injury
- No RBC, protein, or granular casts in urine
- no improvement in renal function with fluid
Treatment:
- splanchnic vasoconstrictors ( midodrine, octreotide, norepinephrine)
- liver transplantation
Hyponatremia ( Na < 135 )
Caused by:
1. Increase ADH
2. Polydipsia, starvation
Clinical:
- confusion, lethargy, muscle cramps, N
Diagnosis:
- measure serum osmolality ( if the measured Sosm, is higher than calculated —> by more than 10-15 mOsm —> indicates an oxygenous osmole diluting the serum sodium.
- correct sodium in hyperglycemia ( sodium correction —> sodium decrease by 1.6 for every 100 elevation in glucose)
Dirty medicine videos nephrotic vs. nephritic
Indication of dialysis:
- Symptoms ( confusion, lethargy, N/V — severe uremic symptoms !!
- Elect. ( potassium = HYPERKALMEIA and acidosis NOT RESPONDING TO MEDICAL MANAGEMENT)
- Volume over load not responding to dieuritic
- Minimal/ No urine output
Renal biopsy is confirmative of CKD
Ratinopathy, for how long
HTN ( for how long)
1. Urine amount + frequency
2. Dysuria + hematuria
3. Have you been seen by nephrology
4. History of NSAIDS —>
5. HAVE YOU BEEN IN HOSPITAL … did they provide you with Intermascular medication
6. History of renal stone ?
7. Did you ever need dialysis before?
Contrast
- SPEP
Anemia
Leukopenia
Hyponatremia
Hypokalemia
BUN/Cr ratio > 30
- urine output decreased —> after holding diuretics
- urine sodium = 5
Microscopic finding on Urinalysis
- broad cast
- Muddy brown cast
- renal tubular necrosis (RTN) - RBC cast
- renal interstitial - WBC cast
- Fatty casts
- Eosinophils
Muddy brown cast in patient with ampho, AG, cisplatin or prolonged ischemia
- acute tubular necrosis
- treat with fluid
- avoid nephrotoxic agent ( contrast dye, ARBs, NSAID)
- DIALYSIS if needed
Protein, blood, eosinophils in urine + fever + rash + who took TM-SMX for past 1-2 weeks
- Acute interstitial nephritis
- stop offending agent
- steroid if no improvement
Army recruit or crush victim with CPK of 50 K + blood on dip, but no RBCs
- Rhabdomyolysis
- test: check K concentration on ECG
- Treat with: Bicarb ( to alkanize urine to prevent precipitation)
Enveloped shaped crystal on Urinalysis
- ethylene glycol intoxication
- Anionic gap metabolic acidosis ( AGMA)
- treat with dialysis or sodium-bicarb, if PH < 7.2
If creatinine level jumped in the 48-72 hours after Cardiac cath or CT
- contrast nephropathy.
- prevent by hydration before or giving bicarb or NAC
Indication for emergent dialysis
- Acidosis
- Electrolyte imbalance —> especially K > 6.5
- Intoxication —> anti-freeze (ethylene glycol) or lithium
- Overload of volume —> symptoms of CHF or pulmonary edema
- Symptoms of uremia —> pericarditis, confusion, itching, blood loss
Chronic kidney disease (CKD)
- Caused by —> 1st DM, 2nd HTN
- death due to cardiovascular disease —> maintain LDL < 100
Complication:
1. HTN, fluid retention ( CHF)
2. Normochromic normocystic anemia —> loss of EPO
3. High K, High PO4, low Ca ( lead to secondary hyperparathyroidism)
4. High PO4 lead to precipitate Ca in tissue —> skin necrosis
5. Uremia —> confusion, pericarditis, itching, blood loss ( due to platelet dysfunction)
Causes of hyponatremia ( too much water)
- Hypervolemic hyponatremia ( gain too much water)
- CHF
- nephrotic syndrome
- cirrhosis - Hypovolemic hyponatremia: (loose too much water)
- diuretics
- vomiting
- free water - Euvolemic hyponatremia:
- SIADH ( check chest xray if smoker)
- addison disease
- hypothyroidism
Treatment:
- IV normal saline (fluid restrict them)
- only use hypertonic saline (3%) if patient have sign/symptoms of seizure or Na concentration of < 120
- avoid treating them fast (ONLY 12-24 mEq/Day)—> to prevent central pontine myelinolysis (CPM)
Causes of hypernatremia
- caused by loss of water
- treat with:
1. Replace water with D5W or other hypotonic fluid
2. Don’t correct fast of else —> patient develop cerebral edema
Hypocalcemia
- numbness
- prolonged QT
Hypercalcemia
- painful bone + renal stones + abdominal groan + psychiatric moans
- shortened QT
Hypokalemia
- paralysis (severe muscle weakness) + ilues + decrease DTR + palpitation + arrhythmia
- ST depression + T-wave flattening followed by U-wave development
- treat with:
1. Oral K ( make sure patient can pee), IV in severe cases
2. Maximum 40 mEQ/ hr
Causes:
1. GI loss ( diarrhea, vomiting, diuretics; thiazide, loop)
2. Medication that causes intracellular K shift —> (beta 2 agonist, insulin)
3. Hypomagnesemia —> ( low mg opens the mg-dependent K Channel spilling K into urine)
Hyperkalemia
- prolonged PR + prolonged QRS + tall peaked T wave + sine wave
- muscle weakness, flaccid paralysis, cardiac arrhythmia, abdominal distention, diarrhea
- Treat with: ( C BIG K Drop)
1. Calcium gluconate ( prevent arrhythmia )
2. Beta 2 agonist (albuterol) or ( sodium bicarb)
3. Insulin ( drive K into cells)
4. Glucose
5. Kayxalate ( poop out K; takes days; outpatients)
6. Last resort —> dialysis, in refractory patient
Caused by: CARED
- Cellular lysis: rhabdomyolysis, burns, tumor lysis
- Decrease Aldosterone: hypoaldosteronism, adrenal insufficiency
- Renal failure
- Excessive K intake ( eating too much banana in dialysis patient)
- Drugs: ACE I/ ARBS, Spironolactone
Acute renal allograft
- T-cell mediated
- occurs within first 6 months following transplant
- asymptomatic rise in serum creatinine
- renal biopsy confirms diagnosis—> lymphocytic infiltration of the intima
- treatment: high dose IV glucocorticoid
Pyelonephritis
- affect transplanted patient
- symptoms: fever + dysuria + pelvic pain
- finding: nitrate or leukocyte esterase on UA
Acute toxicity to calcineurin inhibitor ( tacrolimus & cyclosporine)
- vasoconstriction of renal afferent & efferent arteriole
- lead to prerenal acute kidney injury + HTN
- BUN/Cr ratio= > 20
Acute renal failure present with hypocalcemia, however if hypercalcemia present this suggest multiple myeloma
multiple myeloma/malignancy:
- anemia + hypercalcemia + bone pain + acute renal failure
Determine which type of acute kidney injury
Prerenal:
- low urine sodium ( < 20)
- elevated BUN/Cr ratio (> 20)
- urine osmolality (> 500 mOsm)
- microscopy (Bland; without WBC, Protein or casts )
Intrinsic
- Acute tubular necrosis (ATN)
- High urine sodium ( > 40)
- normal BUN/Cr (10-15: 1)
- urine osmolality ( almost 300)
Microscopy: muddy brown casts
Post renal:
- hydronephrosis on Ultrasound
Effect of hypovolemia of renin-angiotensin system (RAS)
- Hypovolemia stimulated RAS system
- improve intravascular system & GFR & BP via vasoconstriction & kidney- mediated Na & water resorption
- increased renin + increased efferent arteriolar resistance + increase tubular sodium reabsorption
Acute gallstone pancreatitis
- colicky abdominal pain after eating
- severe epigastric pain + vomiting + elevated lipase
- pancreatitis lead to hypovolemia:
1. Activates RAS system
2. Increase renin secretion
3. Lead to: - vasoconstriction: increase efferent arteriole resistance= improve GFR & BP
- sodium retention: increase sodium reabsorption at the proximal convoluted tubules
- aldosterone production: reabsorption of sodium & water at the distal convoluted tubules
Metformin
- used in diabetes type 2
- can cause: lactic acidosis, diarrhea, vitamin B12 deficiency
- metformin should be withhold in the sitting of AKI ( Dehydration, decrease mucous membrane, increase Bun/Cr > 20)
- metformin is avoided in Chronic kidney disease ( GFR < 30)
- Sepsis ( fever + hypotension + tachycardia) & dehydration = increase lactic acid levels
Pre-renal AKI
- result from total body-volume depletion
- it can occur in volume-overloaded states that involves ( reduced effective arterial blood volume) —> due to acute heart failure exacerbation & AKI is most likely due to cardiorenal syndrome
Cardio-renal syndrome
LV & RV failure
- Decrease CO
- decrease renal perfusion
- decrease GFR
- activates RAS system
- vasoconstriction + aldosterone production + increase sodium/water reabsorption
- LV & RV failure
- Increase central venous & renal venous pressure
- decrease glomerular capillary filtration gradient
- decrease GFR
- activates RAS system- vasoconstriction + aldosterone production + increase sodium/water reabsorption
- LV & RV failure
- vasoconstriction + aldosterone production + increase sodium/water reabsorption
Renal venous congestion & AKI in cardio-renal syndrome
- Increase renal venous pressure
- Increase vasa recta fluid leakage
3.Tubulo-interstitial edema —> increase intratubular pressure
- Increase Bowman capsule hydrostatic pressure —> decrease filtration gradient —> decrease GFR
Diuretics are the most effective therapy for AKI due to cardiorenal syndrome
- furosemide (lasix)
Crystal- induced AKI (renal tubular obstruction)
- EXAMPLES:
- Acyclovir
- Sulfa
- uric acid
- methotrexate - increase risk with volume depletion & CKD
- Diagnosis:
- on UA: hematuria ( RBC in urine) + pyuria ( WBC in urine) + crystals - Management:
- discontinue drug
- volume repletion
- loop diuretics ( furosemide)
Work-up of high anion- gap metabolic acidosis
- High anion gap metabolic acidosis (MUDPILES)
- associated clues
- Drug ingested
- salicylate ( early respiratory alkalosis)
- Isoniazid
- Iron - Hypoperfusion
- increase lactic acid —> lactic acidosis ( example Metformin in DM2 avoid in CKD) - Renal failure:
- increase BUN —> uremia ( confusion, pericarditis, itching, blood loss) - Hyperglycemia:
- urine & serum ketones —> diabetic ketoacidosis - Osmolal gap:
- ethylene glycol ( urinary calcium oxalate crystal; renal failure)
- methanol ( blindness)
- propylene glycol
Note: (MUDPILES)
Methanol, uremia, DKA, propylene glycol, isoniazid/Iron, lactic acid, ethylene glycol, salicylate
Analgesic nephropathy
Patho:
- prolonged use of combination analgesics
1. Acetaminophen
2. Aspirin/NSAIDs
- manifest as “chronic interstitial nephritis ± papillary necrosis”
Clinical:
- chronic pain ( headache, lower back pain)
- malaise, fatigue, flank pain
- UA: WBC + WBC cast ± mild proteinuria
- hematuria & urine RBC, if papillary necrosis present
- imaging: small kidney ± papillary calcification & irregular contour
Rhabdomyolysis
Etiology:
Skeletal muscle lysis/necrosis due to:
1. Crush injury or prolonged immobilization
2. Intense muscle activity ( seizure, excretion)
3. Drug/medication in-toxicity ( statin)
4. Alcohol abuse + cocaine abuse
Clinical:
1. Muscle pain/weakness
2. Dark urine ( myoglubinuria/ pigmenturia)
3. Presence of blood in UA, absence of RBC on microscopy
4. Increase serum K & PO4, decrease Ca
5. Increase AST > ALT
6. AKI
Diagnosis:
- serum Creatinine Kinase (CK > 1000)
Management:
- aggressive IV fluid
- sodium Bicarbonate
Patient with COPD develops pulmonary HTN & cor Pulmonary
- COPD ( dyspnea + cough + wheezing + hypoxia) + chronic respiratory acidosis ( high CO2; from CO2 retention) + compensatory metabolic alkalosis ( high bicarb + near normal pH)
- Pulmonary HTN & cor pulmonary ( JVD, hepatomegaly, peripheral edema in the presence of clear lung)
- In Cor pulmonary —> loop diuretics (furosemide) is used to lower right ventricular filling volume & reduce peripheral edema
- Loop diuretic can lead to hypovolemia, low CO, renal hypo-perfusion —> prerenal azotemia/ AKI can develop
- elevated creatinine ( double of baseline)
- BUN/Cr ratio > 20
- elevated Anion Gap Metabolic Acidosis ( > 14) - Diuretics can cause hypokalemia, but AKI negates that effect explaining the stable potassium level ???
Sepsis lead to prerenal AKI
- Sepsis ( hypotension, tachycardia, altered mental status, leukocytosis, lung consolidation) due to community acquired pneumonia
- Sepsis lead to peripheral vasodilation ( hypotension) & volume depletion ( decrease appetite, decrease oral intake, dry mucous, hypernatremia)
- Sepsis + volume depletion = prerenal AKI ( due to decrease renal perfusion)
Note:
- Renal hypoperfusion —> decrease GFR —> Increase creatinine —> activates RAS —> increase sodium reabsorption —> urine sodium < 20 & low fractional excretion of sodium (<1) —> urea passively follow sodium & water reabsorption —> increase BUN/Cr (> 20) —> urine sediment is bland ( no WBC, no protein, no casts)
- Treatment: IV fluid ( crystalloids)
Contrast- associated AKI
- Creatinine elevation 24-48 hours after arterial contrast, followed by gradual return to baseline (in 3-7 days)
- patient with CKD are at increased risk
- preventative measures include: IV (0.9% saline), avoid NSAIDS, use of smallest possible volume of contrast
Chronic kidney disease (CKD)
- Lead to unintentional weight loss in elderly
- Watchful waiting + nutritional supplement
- Platelet dysfunction is the most common cause of abnormal hemostasis ( easy bruises, non-palpable purpura). PT & PTT are normal. Platelet count is normal or mildly low.
What is the most common cause of nephrotic syndrome in children
- minimal change disease
IGA nephropathy is precedded by what type of infection ?
- upper respiratory infection (± GI infection)
Describe the finding on biopsy in a patient with rapidly progressive Glumerulonephritis ?
- crescent formation
( like a moon)
Young patient ( 7 year old) + Dark urine + puffy face + Sick a couple of days ago + positive ASO titer ?
What type of infection happened in the past 10-14 days ?
- Group A strep infection
- lead to post-strep glomerulonephritis
- Coca-cola urine
- Periorbital edema
- Common in 5-12 years old males
- Positive ASO titer
What is the most common etiology of Acute interstitial nephritis ?
Drug hypersensitivity ( antibiotics, NSAIDS)
What is the most common cause of ESRD
- DIABETIC MELLITUS
Fatty casts or oval fat bodies are commonly associated with what renal disorder ?
- Nephrotic syndrome
Middle age man ( 45 years) + history of HIV + history of heroine use + bubbly urine + swelling in the leg + HTN + fatty casts on microscopy.
What is the likely etiology of the symptoms seen ?
- nephrotic syndrome —> Focal segmental Glomerulosclerosis (FSG)
Signs:
- middle age man
- frothy urine (from proteinuria)
- generalized edema
- seen with: HIV + Heroin use + HTN
Kidney stones & BPH are both common causes of which type of acute kidney injury
- post-renal AKI
- obstructive uropathy ( from Bladder neck obstruction from BPH)
What is the first line treatment for patient with acute tubular necrosis ?
- supportive ( IV fluid + discontinue of any offending agent)
What 2 types of HTN medication classes reduce proteinuria seen in renal disease?
- ACE inhibitors (-pril)
- ARBs (-sartan)
- used in DM patients —> have a vasodilation effect on efferent arterioles
What type of acute glomerulonephritis has positive anti-GBM antibodies that attack the type 4 collagen in the glomerular basement membrane ?
- Goodpasture syndrome ( Anti- GBM disease)
Signs:
- hematuria + hemoptysis
What type of nephrotic syndrome has glomerular basement membrane thickening seen on renal biopsy ?
- membranous nephropathy
What type of AKI is seen in volume depleted patients, such as patients with a history of diarrhea, vomiting & blood loss?
- pre-renal AKI
Elderly + hematuria + smoking + left sided varicocele is palpable .
What diagnosis ?
Renal cell carcinoma (RCC)
- left kidney mass = obstruct proximal left gonadal vein = lead to distal left varicocele
Elderly man + with AKI after CT with contrast + urinalysis shows muddy brown casts
What type of AKI ?
- Acute tubular necrosis (ATN)
- also seen with: vancomycin or aminoglycosides
Middle age patient + persistent flank pain + BP running high for sometimes + bilateral palpable flank mass.
Likely diagnosis?
- polycystic kidney disease
Symptoms:
- bilateral abdominal mass + flank pain
A BUN/Cr ratio > 20: 1 should make you suspect which type of AKI?
- pre-renal AKI
( due to dehydration, hypovolemia)
Elderly women + elevated K of 6.3 + no ECG abnormality + patient is asymptomatic + history of phlebotomy struggling before drawing blood + multiple needle sticks + the tourniquet was placed for so long her finger turned blue
Causes of elevated K level?
- psuedo-hyperkalemia
—> lead to RBC hemolysis during blood withdraw
At what stage & GFR level is ERSD defined ( AKA kidney failure)?
At stage 5 ( GFR < 15) (Dialysis is required)
A patient with history of turner syndrome & nephrolithiasis (kidney stone) presents with third UTI in the last 6 months.
What abnormality will be likely seen on CT urography ?
Horseshoe kidney ( fusion of the poles of the kidney) ( U-shaped kidney)
Symptoms:
- recurrent UTI
- recurrent kidney stones
- seen in turner syndromes
Elderly male ( 68 yr) + history of hyperlipidemia, HTN, 2 coronary stents + on 3 different HTN medication ( amlodipine, lisinopril, hydrochlorothiazide) + BP today is elevated (174/96) + abdominal bruits heard
What is likely found on CT angiography of the abdomen/pelvis ?
Renal artery stenosis
Sign:
- persistent HTN ( unresponsive to 3 different HTN medication)
What is the first line medication for patient with minimal change disease?
Glucocorticoid
Middle age man ( 49) + fever + rash on abdomen+ recent history of lower back sprain + prescribed naprosyn for pain + increase Cr level + increase eosinophilia + urinalysis shows WBC casts
Initial treatment for patient?
- acute interstitial nephritis (AIN)
Treatment:
1. Discontinue offending agent ( Naprosyn = NSAID) —> lead to drug hypersensitivity
What type of renal disorder can lead to extra-renal manifistation such as cerebral aneurysm & mitral valve prolapse ?
- polycystic kidney disease
Symptoms:
- Autosomal dominant
- abdominal pain + flank pain
- increase risk for cerebral aneurysm (subarachnoid hemorrhage) & MVP
What classic finding will be seen on ECG in a patient with hyperkalemia early on ?
Early:
- tall peaked T wave ( with shortened QT interval)
Progress:
- prolonged PR interval + prolonged QRS
Severely ill:
- Sine wave
What is the first line outpatient empiric treatment option for Acute pyelonephritis, as long as there is no resistance or contraindication to this class ?
- fluoroquinolone (ciprofloxacin, levofloxacin)
- for outpatient empiric treatment —> once culture result is received —> change treatment to suit the culture !!
What is classic triad can be seen in patient with Renal Cell Carcinoma in advanced disease ?
Triad:
- palpable abdominal mass + flank pain + hematuria
A patient with pH of 7.27, PCO2 of 56 & HCO3 of 24 has what type of acid base disorder ?
- primary respiratory acidosis uncompensated
What electrolyte abnormality should be suspected in a patient with T wave flattening & prominent U wave development on ECG ?
Hypokalemia
what medication is used in patients with hyperkalemia to stabilize the myocardium & decrease incidence of cardiac arrhythmia
- IV calcium gluconate
A patient that rapidly responds to IV fluid administration, with normalization of serum creatinine in 24 to 72 hours is considered to likely have which type of acute kidney injury ?
- prerenal AKI
What is the most common site of metastasis in the renal cell carcinoma
- Lung
- followed by bone, lymph nodes
Diffused effacement or loss of the epithelial cell ( podocytes) foot process is a classic finding on electrone microscopy in what type of nephrotic syndrome ?
Minimal change disease
What is the most common type of renal cell carcinoma ?
- clear cell
What is the most common bacterial organism found in acute pyelonephritis ?
- E.coli (80%)
Beside the kidney, what area of the body does Goodpasture syndrome commonly affect ?
Lungs
Before initiating treatment in patient with hypokalemia, what other electrolyte should you check to ensure there will not be resistance to the potassium replenishment ?
- Magnesium
Central pontine myelinolysis ( AKA: osmotic demyelinating syndrome) can be a serious consequence of rapidly correcting which type of electrolyte abnormality?
- hyponatremia
What compensatory mechanism do the lungs employ to counteract metabolic acidosis
- increasing the respiratory rate (hyperventilate) —> - respiratory alkalosis
What finding on microscopy are indicative of acute glomerulonephritis ?
- RBC casts
Elderly male (76 yrs) + with ESRD (stage 5 of CKD) + symptoms of vomiting, weight loss, muscle cramps, fatigue, altered mental status
What is the most common cause ?
- Uremia
- elevated concentration of Urea in the blood
A 71 yr old female present with severe muscle weakness, and N/V + Loss of DTR + ECG shows decreased T wave amplitude + currently taking furosemide ( loop diuretic) for CHF.
Replenishing of what electrolyte is needed ?
- potassium replacement ( she has hypokalemia)
A nepphroblastoma (wilm’s tumor) can be differentiated from neuroblastoma by what physical exam finding ?
- The mass in a nephroblastoma (wilm’s tumor) rarely cross the midline of the abdomen
- unlike a neuroblastoma which commonly crosses the midline
Elderly woman (62 yrs) + weakness & palpitation + ECG shows tall peaked T wave & shortened QT interval + history of Diabetes, HTN, Hyperlipidemia + medication ( metformin + rovastatin + lisinopril)
Which medication is the most probable offending agent leading to her symptoms?
- patient have hyperkalemia
- lisinopril ( ACE-inhibitor) is the cause
Urinary outflow obstruction that leads to dilation & distention of the renal collecting system of one or both kidney is known as ?
Hydronephrosis
What is the gold standard/ definitive test to diagnose renal artery stenosis ?
- renal arteriography ( diagnostic & therapeutic)
- can diagnose it and stent the artery at same time
CKD is defined as the presence of kidney damage or decreased kidney function ( eGFR < 60) for at least how many months ?
Three or more months
- to differentiate CKD from AKI
Methanol, uremia,DKA, propynele glycol, isoniazid/iron, lactic acid, ethenyle glycol, salicylates
causes what type of acid base disorder ?
- anion gap metabolic acidosis
What is the most common renal malignancy in children ?
Nephroblastoma ( Wilm’s tumor)
Bleeding types
- CKD —> easy bruising + non-palpable purpura + due to platelet dysfunction. normal PT, PTT. Normal or mildly low platelet count
- hemophilia A ( factor 8 deficiency) —> easy bruising + prolonged PTT
- DIC —> bleeding + risk of sepsis or trauma + prolonged PT & PTT
- vasculitis —> palpable purpura
Note:
- non-palpable purpura seen with platelet or coagulation disorders
Calciphylaxis ( calcific uremic arteriolopathy)
- systemic arteriolar calcification & soft-tissue calcium deposition with local ischemia & necrosis
- commonly seen in patient with longstanding ESRD
- risk factors include: hyperparathyroidism, hyperphosphatemia, hypercalcemia ( often serum Ca is normal)
Rheumatic arthritis ( chronic inflammation) —> lead to AA amyloidosis —> lead to nephrotic syndrome
- Nephrotic patient ( proteinuria, pitting edema, hypoalbuminemia)
- Present with rheumatoid arthritis ( swan neck deformity, ulnar deviation, nodules)
- Complicated with AA amyloidosis
Note:
- AA amyloidosis can develop in the setting of chronic inflammation ( long standing Rheumatic arthritis)
- the most common manifestation of AA Amyloidosis is:
- Renal disease ( proteinuria or nephrotic syndrome)
- laboratory shows: elevated ESR + normocytic anemia
- histology reveals:
1. Amorphous hyalin material that is stained in Congo-red
2. Green birefringence is noted under polarized light
Common cause of nephrotic syndrome in adults
- membranous nephropathy (glomerulopathy)
- Focal segmental Glomerulosclerosis
- Amyloidosis
Two types of amyloidosis
AA Amyloidosis
- associated with inflammatory conditions ( Rheumatoid arthritis & Inflammatory bowel disease; PU)
- associated with chronic infection: TB, osteomyelitis
AL Amyloidosis
- associated with Multiple myeloma
- associated with W. Microglobulinemia
First line therapy for renal artery stenosis ?
- ACE- Inhibitors (-pril)
Or - ARBs ( -sartan)
- patient with renal artery stenosis & on ACE-inhibitors are less likely to develop MI, stroke, ESRD.
BUT, have high risk for AKI. Thus, renal function must be monitored closely
Unilateral vs. bilateral renal artery stenosis
Unilateral renal artery stenosis:
1. Affected kidney has reduced renal blood flow & GFR
2. The healthy kidney compensate. Thus, lead to low acute changes in GFR
Bilateral renal artery stenosis:
1. Affected kidneys have reduced renal flow & significant low GFR. Patient can only tolerate ACE or ARBs only if creatinine rise < 30%
Second line of treatment to patient with renal artery stenosis
- Renal artery stent
Or - Surgical Revascularization
Only use when:
1. Reserved for patient with resistant HTN
2. recurrent flash pulmonary edema
3. refractory heart failure due to severe HTN.
Hypertensive nephrosclerosis
- develop in patient with uncontrolled HTN
- characterized by hyaline arteriolosclerosis & ischemic glomerulosclerosis
- feature:
1. Elevated CR ( due to decrease GFR)
2. Ultrasound shows small, atrophic kidney
3. Bland ( no WBC, no RBC) urinalysis with mild proteinuria
Dialysis-related amyloidosis
- inadequate removal/clearance of beta-2 microglobulin despite dialysis
- present with shoulder pain/hypertrophy + Carpal tunnel syndrome + bone cysts
Peritoneal dialysis-related peritonitis
- caused by:
1. touch contamination of the dialysis catheter lumen with skin bacteria
Or
2. Extension of a localized skin infection at the catheter site
Common organisms:
1. Staph. Epidermidis
2. Staph. Aureus
Diagnosis:
- abdominal pain + cloudy fluid
- neutrophil on fluid analysis
- positive fluid gram stain or culture
Treatment:
- combination of (vancomycin & gentamicin)
—> empiric treatment covers both (+) & (-) gram bacteria
Relationship of diabetic nephropathy to ESRD
Measured via:
1. Urine Albumin to Creatinine ratio
- normal: <30
- microalbuminuria: 30-300
- macroalbuminuria: >300
Diagnosis of DN:
1. Persistent (more than 3 month) or elevated albuminuria (>30)
- Patient with diabetes can have diabetic nephropthy as micro vascular complication that can lead to ESRD.
- UACR should be measured at initial diagnosis of DM type 2 or at 5 years after diagnosis of DM type 2
- Hyperglycemia signs ( polydipsia and polyuria)
Lupus nephritis
Caused by:
-SLE ( fatigue, inflammatory arthritis, anemia, thrombocytopenia)
Clinical:
Shows both:
1. Glomerulonephritis ( hematuria, proteinuria, renal failure, HTN, peripheral edema)
2. Nephrotic syndrome ( proteinuria, hypoalbuminemia, edema)
- Significant protein loss —> low serum albumin —> lower extremity edema + pleural effusion ( dullness on percussion + decreased breath sound)
Diagnosis:
- Positive anti-double standard DNA ( deposits on glomerulus)
Membranoproliferative glumerulinephritis
- Is type of nephrotic-range with hematuria and proteinuria
- persistence activation of alternative complement system and causes kidney damage
-absence of immunoglobulin
Renal venous thrombosis
Present with:
Abdominal pain, fever, hematuria
Associated with: membranous glomerulopathy
SLE
- anemia, thrombocytopenia, leukopenia
- anti-ANCA, anti-dsDNA, anti-smith
- low complement level and high immune complex
Renal vein thrombosis (RVT)
Clinical:
- hematuria + flank pain + scrotal edema ( in men)
NOTE:
- patients with nephrotic syndrome have increase risk for DVT, PE, RVT
- patient with hypoalbuminuemia
Type of stones
- Calcium ( oxalate or phosphate) ( > 75%):
- high sodium or oxalate diet or malabsorption —> oxalate
- renal tubular acidosis ( phosphate)
- small, radiopaque stone
- envelop ( oxalate), wedge (phosphate) - Magnesium ammonium phosphate ( struvite) ( 15%) :
- UTI with urease producing organism ( proteus)
- large, radiopaque stone
- rectangular - Uric acid ( 8%):
- Gout, diabetic/metabolic syndrome, myeloproliferative disorders
- small, radiopaque
- yellow/brown
Risk factor for kidney stone ( calcium oxalate stone):
- dehydration, increase sodium or oxalate in the diet, obesity, hyperparathyroidism, malabsorptive disorders
Rhabdomyolysis
Signs:
- muscle weakness
- dark urine
- decrease urine output
- elevated creatinine
- elevated blood in UA, but no blood in microscopy
- AKI
- associated with:
1. drug myotoxicity ( statin, fibrates, colchicine, cocaine
2. vasoconstriction: cocaine
3. prolonged immobilization compression ischemia : alcohol, opioid, BDZ
Patient with sickle cell trait
- patient don’t have the symptoms of sickle cell disease
- sickling of RBC occurs under phycological stress —> hypoxia, dehydration, acidosis
- lead to renal papillary necrosis with hematuria & possible flank pain
Note:
Complication of sickle cell trait:
1. Hematuria/ papillary necrosis
2. Splenic infarct ( at high altitude)
3. Exertional rhabdomyolysis ( positive myoglubinuria + positive blood in urine + No RBC in urine/microscopy)
4. Renal tubular acidosis ( when urine pH = 5.8) —> tubular damage with impaired H+ secretion
Nephrolithiasis
- acute flank pain + hematuria
- pain radiates to the groin
Management:
-dietary:
1. Increase fluid
2. Reduce sodium
3. Reduce protein
4. Normal Ca intake
5. Increase citrates ( fruits/veg)
-drugs: ( to lower urinary calcium excretion)
1. Thiazide diuretics
2. Urine alkalinization ( potassium citrate/ bicarbonate salts)
3. Allopurinol ( for hyperuricuria-related stones)
Note:
1. Hypercalciuria = when urine calcium excretion > 4 mg/kg
Pyelonephritis
Flank pain + hematuria + urine WBC/Bacteria/nitrites/leukocyte esterase
Glomerulonephritis
Hematuria + Proteinuria + HTN + dysmorphic RBC + RBC casts
- NO acute flank pain
Low urine PH seen with:
- chronic diarrhea
- diabetes/ metabolic disorders
Increase urine concentration seen with:
- dehydration
- hot climate
Increase uric acid secretion in urine seen with:
- gout
- myeloproliferative disorders
If urine pH in low ( less than 5)
- use potassium citrate ( to alkalinize urine)
Bladder cancer
- painless hematuria
- associated with smoking, elderly, carcinogenic chemicals
- malignant transformation of bladder epithelial cells
Diagnosis:
- flexible cystoscopy + biopsy
Treatment:
- no muscle invasion —> TURBT ( transurethral resection of bladder tumor) + intravesical immunotherapy
- muscle invasion—> radical cystectomy & systemic chemo
- metastatic —> systemic chemo & immunotherapy
Bladder infection
- hematuria + suprapubic pain + dysuria + sign of infection ( urine WBC/bacteria/leukocyte esterase/nitrite)
Ureterolithiasis
- epithelial injury due to scrapping of surface by stone
- hematuria + flank pain that radiates to groin + crystal on urinalysis
Glomerulonephritis
- increase permeability of the glomerulus
- allow RBCs to pass into urinary tract from circulation
- symptoms: hematuria + proteinuria + RBC casts ….
Types:
- strep A
- IgA
- RPG
-MPGN
Most common cause of painless hematuria in older people who used to smoke
- bladder cancer
Renal infarction —> caused by endocarditis
Symptoms:
- flank pain + N/V
- hematuria + proteinuria + without casts
- wedge-shaped cortical infarction seen on CT
- Can occur after:
1. Endocarditis ( fever, leukocytosis, cardiac murmur)
Sodium nitroprusside ( for HTN emergency) can lead to cyanide toxicity in patient with renal insufficiency ( high creatinine)
- Metabolic acidosis + neurologic changes ( headache, confusion )
CKD patient taken ACE-Inhibitor or ARBS
- Can develop hyperkalemia
- Treat with Ka-removal from stool ( patiromer)
Hypercalcemia in sarcoidosis
- finding: skin nodules & erythema nodusom
- occurs from extra-renal calcitrioil production in the lung & lymph node & is independent from PTH production
- usually high (calcitriol), low (PTH), high (urinary calcium)
Hypokalemia result from
- Increase intracellular entry via:
- insulin
- beta-adrenergic agonist (albuterol)
- hematopoiesis - GI loss
- renal- Ka wasting:
- hyperaldosteronism
- diuretics
Non-anion metabolic acidosis (Normal anion gap)
( loss of bicarbonate) (between 10-14)
—> (low pH< 7.35) & ( low bicarbonate < 22) & ( compensatory low PCO2)
- Severe diarrhea
- Renal tubular acidosis
- Excess saline infusion
- Intestinal or pancreatic fistula
- Diuretics ( CAI or MRA)
Renal tubular acidosis —> non-anion gap metabolic acidosis (has a normal anion gap )
(Loss of bicarbonate )
Caused by: Impaired urinary acid excretion
Type 1 RTA:
1. Impaired H+ excretion ( being retained) in the distal tubule & can be recognized by inappropriate high urine pH (> 5.5) in the setting of acidosis
2. Hypokalemia
3.Treat with: oral sodium bicarbonate
Type 2 RTA:
1. Impaired bicarbonate reabsorption in the proximal tubule
2. Hypokalemia
3. Treat with: high dose oral/Iv sodium bicarbonate
Type 4 RTA
1. Hyperkalemia + moderate renal insufficiency
2. Occurs in uncontrolled diabetes
Methanol or ethanol ingestion lead to
- High anion gab metabolic acidosis & high osmolal gap
Diabetic ketoacidosis
Lead to metabolic acidosis ( low pH, low bicarbonate) & compensatory respiratory alkalosis ( hyperventilation, low PCO2)
Management of hypercalcemia
( 1. normal saline + calcitonin; 2. bisphosphonate)
- Normal saline + calcitonin
- Avoid loop diuretics (unless
volume overload/heart failure exist)
- Avoid loop diuretics (unless
- Long term —> bisphosphonate
Hyperkalemia caused by
(ACE-I, ARB, NSAID, TMX, K-sparing, heparin…)
- ACE-i & ARBs
- Cyclosporine
- Digitalis
- Heparin
- Non-selective beta adrenergic blocker
- NSAIDs
- Potassium- sparing diuretics (triametrene) & (amiloride)
- Succinylcholine
- Trimethoprim
Familial hypocalciuric hypercalcemia (FHH)
( High Ca, high PTH, low urinary Ca)
- Asymptomatic hypercalcemia
- Normal/elevated PTH
- Low urinary calcium excretion
—> differentiated from primary hyperparathyroidism ( shows high urinary calcium excretion)
—> differentiate from Multiple myeloma & malignancy ( has low PTH)
Pneumonia lead to
- primary respiratory alkalosis (hyperventilation) (High pH, low PCO2)
—> few days after antibiotic treatment, patient can have foul-smelling diarrhea, related to C.difficile —> more severe diarrhea can lead to non-anionic gap metabolic acidosis (loss of bicarbonate)
Hypovolemic hyponatremia management
(Increase renin, increase aldosterone, increase ADH)
Hypovolemia: diarrhea, poor skin turger, hypotension, low renal perfusion
Low renal perfusion —> stimulated RAAS system —> increase renin, increase aldosterone —> this, stimulates ADH to reabsorb sodium & water at distal tubule
Hypercalcemia treatment
Normally,
1. IV hydration + calcitonin
2. Bisphosphonate
Renal insufficiency & heart failure:
1. Hemodialysis
Hypercalcemia due to excessive vitamin intake, granulomatous disease (sarcoidosis), lymphoma
1. Glucocorticoid
Mixed primary acid base disorders
(Sepsis, salicylate toxicity)
( hyperemesis/pregnancy + HF/COPD)
- Metabolic acidosis + respiratory acidosis: sepsis
—> pH is low - Metabolic acidosis + respiratory alkalosis: salicylate toxicity
—> pH is near normal
—> tinnitus + fever + tachypnea
——————
- Metabolic alkalosis + respiratory alkalosis: hyperemesis gradidarum & hyperventilation of pregnancy
—> pH is high - Metabolic alkalosis + respiratory acidosis: overdiureses heart failure & underlying COPD
—> pH is near normal
——
Metabolic acidosis + metabolic alkalosis: DKA with severe vomiting
—> pH is near normal
Hypokalemic, hypochloremic metabolic alkalosis
—> seen with:
1. Gastric suction or severe vomiting
2. Diuretic (loop or thiazide) overuse
—> management:
1. Normal saline
Differential diagnosis of metabolic alkalosis
( high pH > 7.45) & ( high bicarbonate > 24)
- Low urine chloride < 20:
- nasogastric feeding & vomiting
- diuretics
- responsive to normal saline
- High urine chloride > 20:
- with hypovolemia —> bartter & Gitelman syndrome
- with hypervolemia —> excessive mineralocorticoid treatment ( primary hyperaldosteronism, cushing syndrome, ectopic ACTH production)
** unresponsive to normal saline
SIADH vs. diabetic insipidus
SIADH:
1. Hyponatremia + hyperkalemia + hypoglycemia + hypotension + hypovulemia
2. Low serum osmolarity + high urine osmolarity
3. Correct with hypertonic solution
DI:
1. Hypernatremia + hypokalemia
2. High serum osmolality + low urine osmolality
3. Correct with DDAVP (ADH)
Site of action of various diuretics
- Proximal tubule —> CAI —> acetazolamide
- Descending loop of Henle —> osmotic diuretic —> mannitol
- Ascending loop of henle —> loop diuretic —> furosemide
- Distal tubules —> thiazide —> hydrochlorothiazide
- Collecting duct —> potassium-sparing —> Sodium channel blocker ( amiloride) & aldosterone receptor antagonist ( spironolactone)
Evaluation of hyponatremia
- Serum osmolality > 290:
- hyperglycemia
- marked renal failure - Urine osmolality < 100:
- primary polydipsia
- malnutrition (beer drinker’s potomania) - Urine sodium < 25:
- volume depletion
- CHF
- cirrhosis - Urine sodium > 25
- SIADH
- adrenal insufficiency
- hypothyroidism
Hypomagnesemia can be seen with hypokalemia and hypocalcemia (in alcoholic use disorder)
- lead to refractory hypokalemia ( seen in patient with hypokalemia that is difficult to correct with potassium replacement)
- lead to hypocalcemia due to suppression of PTH
PH & CO2 from ABG
- are best measurement for acid-base status
- HCO3 can be calculated from H-H equation
Respiratory alkalosis
( pH is high) ( PCO2 is low ) ( HCO3 is low)
—> kidney compensate for respiratory alkalosis by excreting bicarbonate in urine —> this alkalize urine —> gives high urine pH
