Nephrology notes

 Acute kidney injury:

 Classification:
- Pre-renal:
o MCC (60-70%). Reversible, caused by low renal blood flow & perfusion
o Causes:
 Hypovolemia (dehydration, diarrhea & vomiting, CHF, hemorrhage, diuretics)
 Hypotension (sepsis, anti-HTN, dehydration), renal artery obstruction, cirrhosis
 Drugs (NSAIDS (afferent constrictor), ACE inhibitors/ARBs (efferent dilator))
o S&S: dry mucus membrane, tachycardia, hypotension, oliguria/anuria
 Anuria: urine output <50-100 ml/day, oliguria: <400-500, polyuria: >3 L/day
o Lab:
 Urine osmolality > 500 mOsm, urine Na <20, BUN:Cr ration > 20:1, scant sediment
 Na fractional excretion (FENa) < 1% (FENa = (Una * PCr * 100) / (PNa * UCr))
- Renal “interstitial”: 25-40%, damage to kidney tissue
o Causes:
 Tubular disease: acute tubular necrosis “ATN” (proximal tubule, thick ascending)
 ischemic ATN: sever low renal perfusion e.g.: shock, sepsis, DIC, hemorrhage
 nephrotic ATN:
drugs: aminoglycosides, NSAIDs, vancomycin, metformin, PPI
toxins: rhabdomyolysis (hyper K, hyper Po4, hyperuricemia), contrast media
 pre-hydration with IV NS/bicarbonate > less risk of contrast nephropathy
 Glomerular disease: good pasture, PSGN, Wegner syndrome
 Vascular disease: renal artery occlusion, TTP, HUS
 interstitial: acute interstitial nephritis (drug-induced (aspirin) or pyelonephritis)
o S&S: depend in the cause but mostly edema
o Lab:
 Urine osmolality <350 mOsm, urine Na > 40, BUN:Cr ration <20:1, FENa >2-3%
 granular cast (ATN), RBC cast (glomerular), fatty cast (nephrotic), eosinophiluria
- Post-renal: obstruction of any urinary tract segment
o Causes: Benign prostatic hyperplasia “BPH” (most), nephrolithiasis, neoplasm
o Diagnosis:
 Test: physical examination, US, catheter
 Lab: early stage: Una <20, FENa >1%, urine osmolality >500, BUN:CR ration < 15:1
 late stage: same as ATN
 Diagnosis:
- Blood: high Bun & Cr, electrolytes, albumin
- Urinalysis:
o Urine dipstick: if protein +: acute glomerulonephritis or acute interstitial nephritis
o Microscopic examination for casts
- Renal US/CT/MRI/doppler: for obstruction and asses the severity
 Complication:
- Infection (MCC of death 75%), CVD, pulmonary edema (give furosemide)
- Hyper K (insulin +/- glucose, sodium sulfate, loop diuretics), anemia
- Metabolic acidosis with high anion gap (give NaHCO3), hypo Ca (no vit D activation)
 Treatment:
- General:
o Avoid drugs that decrease the RBF or nephrotoxic, adjust medication dose
o Correct fluid-imbalance & monitor by daily weight measurement & intake-output
o Dialysis: in case of symptomatic uremia or uncorrectable acidosis
- Prerenal: Tx underlying cause, give NS (restore BP) // Renal: if oliguria > furosemide
- Post-renal: bladder catheter

 Chronic kidney injury:

 Decrease renal function (GFR < 60 ml/min) or kidney damage > 3 months
 Causes: DM (MCC 30%), HTN (25%), chronic GN, interstitial nephritis, polycystic kidney
 Staging:
- I: GFR ≥90 ml/min (hematuria, proteinuria, albuminuria, or increase echogenicity)
- II: GFR: 60-89 ml/min // III: GFR: 30-59 ml/min // IV: FGR: 15-29 // V: GFR ≤ 15
 S&S:
- CVS: HTN (salt & water retention), CHF (volume overload), pericarditis
- GI: nausea, vomiting // heme: normocytic normochromic anemia, bleeding
- CNS: confusion, peripheral neuropathy, asterixis, waddling gait, uremic seizure
- Skin: pruritis, calciphylaxis, hyperpigmentation (muddy face), half-half phenomena
- Electrolytes:
o hyperphosphatemia (less clearance, will decrease Vit d > hypo Ca & 2ry hyper PTH)
o 2ry hyper PTH (renal osteodystrophy), hyper K, hyper Mg, metabolic acidosis
 renal osteodystrophy (osteitis fibrosa, osteoporosis, osteomalacia)
 1ry hyper PTH (low PO4 & high Ca), 2ry (high PO4 & low Ca), 3ry (both high)
 Diagnosis:
- Urinalysis (sediments), measure Cr clearance & GFR, US (kidney size & obstruction)
- CBC (low Hb/RBC, WBCs & PLT dysfunction), electrolytes
 Treatment:
- Diet (low protein & salt), strict control of Bp & blood glucose, smoking cessation
- ACE inhibitors (captopril): dilate efferent arteriole, slow progression, risk of hyper K
- Erythropoietin (anemia), cholestyramine (pruritis), diuretics (pulmonary edema)
- Hyper PO4:
o 1st phosphate binders (Ca binder (Ca carbonate, Ca acetate), non-ca (sevelamer))
o 2nd if low Ca: add active vit D // 3rd if remain high PO4: cinacalcet
- Hyper K:
o If k>7 or ECG changes: 1st choice is Ca gluconate
o If not: glucose/insulin > B1 agonist > resonium, hemodialysis (last option)
- dialysis: either hemodialysis or peritoneal dialysis
- Transplant is the only treatment for half-half phenomena
 Glomerulonephritis:
1. Nephrotic syndrome:
 Proteinuria > 3.5 g/day or +3, hypoalbuminemia, edema, hyperlipidemia (cholesterol)
 Types:
a. Minimal change disease (MCD):
- MC type, mostly idiopathic, mostly in child, associated with Hodgkin & non-Hodgkin
- EM: foot process effacement & podocyte effusion // - LM & IF // good prognosis
- Selective proteinuria (albumin) // Tx: steroid (response well)
b. Focal segmental glomerulosclerosis (FSGS):
- More in adult & African American, hematuria & HTN present, fair prognosis
- Causes: idiopathic, SLE, HIV, heroin, huge loss of nephron
- Tx: steroids (can be resistant), cytotoxic agents, immunosuppressive (azithromycin)
c. Membranous glomerulonephritis: “thick GBM with subepithelial IG deposition”
- 2ry to inf. (HCV, HBV, syphilis, malaria), drugs (captopril, penicillin, aminoglycosides)
- complication: renal failure (33%), renal vein thrombosis
- Tx: treat the cause, 2 corticosteroids, immunosuppressive
d. Membranoproliferative GN: “thick basement membranes & high cellular elements.”
- Causes: HCV & HBV inf. (most), syphilis, lupus (low C3 &C4), C3 convertase (type II)
- Complication: poor prognosis, renal failure (50%), develop HTN, no steroid response

2. Nephritic syndrome:
 Proteinuria < 3.5 g/day, edema, hematuria, HTN, oliguria & azotemia
 Types:
a. Post-streptococcus GN (PSGN):
- MC type, after S. pyogens inf., H/O URTI 2 weeks before or impetigo 6 weeks before
- Tx: mostly self-limited // complication: risk of RPGN // high anti-streptolysin O titer
b. Rapidly progressive “crescentic” GN (RPGN):
- Types:
o I “good pasture syndrome” “anti-GBM”:
 Affect IV collagen, can affect the lungs (hemoptysis, cough, SOB)
 Tx: plasmapheresis (remove anti-IgG Ab), cyclophosphamide & steroids
o II “IgA nephropathy” “Berger disease”:
 MCC of glomerular gross hematuria, H/O inf. Within 2-3 days, mostly in child
 If C3 level is normal (IgA or HSP), if low (MPGN or SLE)
o III “Wegner granulomatosis”:
 Vasculitis, also affect resp. (hemoptysis, cough, sinusitis), epistaxis, conjunctivitis
 Lab: high ESR & + C-ANCA // Tx: cyclophosphamide, steroids, plasma exchange
- Prognosis: poor, can lead to AKI // Tx: anticoagulant (fibrin), immunosuppressive
c. Hereditary nephritis “Alport syndrome”
- X-linked or AD inheritance, abnormal IV collagen, diagnosed by skin/kidney biopsy
- S&S “can`t see, can`t pee, can`t hear a pee”:
o hearing loss (@ adultness), hematuria, visual abnormality, pyuria
 S&S: edema (preorbital then peripheral), xanthoma, leukonychia, PE, ascites
 Diagnosis: 24-hr urine collection, urine dipstick, BUN, electrolytes, CXR, US
 Tx: mostly all types are initially treated with steroids

 Tubulointerstitial diseases “TID”:

1. Acute interstitial nephritis:
 Causes:
- Allergic reaction to drugs (penicillin, cephalosporin), strept. Or legionella infection
- Sarcoidosis, autoimmune (SLE, Sjogren)
 S&S: can present as AKI, rash, fever, pyuria & hematuria
 Diagnosis: RFT (high BUN & Cr), urinalysis (eosinophilia-diagnostic), biopsy
 Treatment: stop causative agent, Tx inf. (Abx), +/- steroids
 Chronic form: characterized by fibrosis & atrophy

2. Renal papillary necrosis:

 Causes: Analgesic nephropathy (NSAIDS, aspirin, Panadol), DM, SCD, UTI, alcoholism
 S&S: back pain, dysuria, cloudy urine, fever
 Diagnosis: excretory urogram
 Complication: obstruction via sloughed or necrotic papillae
 Treatment: trop underlying cause

3. Differences between GN & TID:

 TID is acute while GN is chronic // GN causes nephrotic syndrome while TID don`t
 Steroids and immunosuppressive are mainly used for GN // TID mainly cause by toxins

 Renal vascular diseases:

1. Renal artery stenosis “renovascular HTN”:
 Stenosis > less perfusion > + renin-angiotensin system > secondary HTN
 Causes: atherosclerosis (most) or fibromuscular dysplasia (mostly in young females)
 S&S: HTN (sudden, malignant, progressive, not relieved by drugs), ABD bruit
 Diagnosis: Renal angiogram (gold standard), MRA (more sensitive & specific), doppler
 Treatment: percutaneous transluminal renal angioplasty (PTRA), bypass surgery

2. Renal vein thrombosis “RVT”:

 Causes: nephrotic syndrome (membranous), pregnancy, OCP use, cancer
 S&S: flank pain, HTN, hematuria & proteinuria
 Diagnosis: renal venography or intravenous pyelogram (IVP)
 Treatment: anticoagulant (to prevent PE)

3. HTN nephrosclerosis: (2nd MCC of ESRD)

 Benign: afferent arteriole thickening, high Cr, microscopic hematuria, proteinuria
 Malignant: rapid loss of function, high Cr, papilledema, CNS finding, hematuria
 Treatment: control HTN

4. Sickle cell nephropathy:

 Sickled RBC can cause occlusion > infarction > papillary necrosis/renal failure/UTI
 Treatment: ACE inhibitors

5. Diabetic nephropathy: (best early scan is urine microalbuminuria)

 Early stage: hyperfiltration due to efferent narrowing & afferent dilation
 Late stage: hypofiltration due to efferent and afferent narrowing
 Treatment: it can`t be stopped but only slow the progression
- ACEI & ARBs: decrease progression & control HTN by dilating efferent
- Ca channel blocker (diltiazem), alpha blocker (prazosin), Beta Blocker (atenolol)

 Dialysis:
 Indications:
- 3 clinical: pulmonary edema (volume overload), uremic pericarditis/encephalopathy
- 3 labs: sever metabolic acidosis, severe persistent hyper K, rapid Cr increase
 Hemodialysis:
- Frequency: 3-5 hr. for 3 times/week
- Access:
o Central catheter: Seldingher technique // e.g. subclavian, JV // temporary
o Tunneled catheter: subcutaneous to decrease inf. Risk // temporary
o AV fistula:
 mainly in brachiocephalic // palpable thrill & audible bruit // permanent
- Alternative: Continuous arteriovenous/venovenous hemodialysis
- Advantages: more efficient, initiated faster
- Disadvantages & complications:
o Hypotension, hypoosmolality, inf. Risk, cramps, itching, PE risk, coagulopathy
o Aneurysm, CHF, ischemia & gangrene (all of these are more with AV fistula)
- CI: Pt refuse, severe cardiac disease, end-stage liver disease, advanced malignancy
 Peritoneal dialysis:
- Frequency: once every 4-8 hr. in CAPD & once every 1 hr. in acute
- Access: permanent implanted catheter in peritoneal cavity (temporary in acute)
- specific indications:
o young/infant, CVS/hemodynamically unstable, high risk with anticoagulant
o hemodialysis patient with vascular access failure
- Advantages: pt. can do it alone & in his house, more physiologically like kidney
- Disadvantages & complication:
o High-glucose content (risk of hyperglycemia & hyper TG), ABD/inguinal hernia risk
o Peritonitis (cloudy peritoneal fluid, prevented by sterilization, intra-peritoneal Abx)
- CI: pregnancy, fibrosis of the area, same CI of hemodialysis, recent ABD surgery
 Limitation: no synthetic function (risk of vit D & erythropoietin deficiency)
 Disequilibrium syndrome:
- Occur when rapid correction of electrolytes by dialysis that will lead to imbalance
btw CSF & blood > higher CSF pressure & osmolality > fluid shifting > coma & death
 other information:
- Pt. on hemodialysis should be given heparin to prevent clotting
- Pt. should measure his/her weight before & after dialysis (fluid balance)
- Flushing of peritoneal cavity is done in case of presence of blood in the catheter
- GFR calculation: Cockcroft-Gault: (140-age) * IBV/SCr * 72

 Polycystic kidney disease:

1. AD PSKD:
 S&S: hematuria, HTN, palpable kidney, ABD pain, signs of infection
 Diagnosis: US (best & confirmatory), CT & MRI, genetic (last option)
 Complication:
- MC genetic cause of CKD, 50% of pt. will develop ERSD, nephrolithiasis
- Intracerebral berry (aneurysm), mitral valve prolapses
 Tx: no cure, drain cyst, Tx inf., control HTN (ACEI)

2. AR PSKD:
 S&S: portal HTN, cholangitis, palpable kidney, HTN, pulmonary hypoplasia
 Diagnosis: US (also hepatomegaly), molecular genetic test // Tx: no cure, manage S&S

 Kidney transplant:
 Anatomy: kidney will be inserted in the Rt. Iliac fossa (iliac artery/vein anastomosis)
 Immunosuppression:
- Induction: high dose, mainly for high risk pt. (e.g. pregnant, young age)
- Maintenance:
o anti-inflammatory (prednisolone), anti-metabolite (azathioprine), tacrolimus
 Post-transplant complication:
- Acute rejection:
o Types:
 Cellular: within 10 days, give pulse steroid & anti-thymocyte globulin (ATG)
 Ab mediated: within 3-7 days, plasmapheresis + IVIG, rituximab
 Hyperacute: in the theater, do nephrectomy & plasma exchange
- Infection: CMV & P. jeroveci (1st month), herpes (1-6 months)
- Chronic allograft damage: MCC of transplant failure
- Malignancy: Kaposi (stop cyclosporin & give other immunosuppressive)
- Other: recurrence (MPGN or FSGN mostly), HTN, DM, delayed graft function (ATN)

 acid-base balance:
1. respiratory acidosis:
 low blood PH with high PaCo2 +/- renal compensation:
- acute: HCO3 should increase 1 mmol/L for every 10 mmHg increase in PaCO2, *
- chronic: HCO3 should rise 4 mmol/L for every 10 mmHg increase in PaCO2, **
 causes:
- respiratory (COPD, obstruction, muscle fatigue), neuromuscular (myasthenia)
- drug-induced (morphine, anesthesia, sedative, narcotics), CNS (brain stem injury)
 S&S: somnolence, confusion, asterixis, headaches, papilledema, clubbing (chronic)
 treatment:
- if PaO2 is low (<60 mmHg): O2 supplement (in COPD use venturi mask till 88-92%)
- correct reversible causes, bronchodilator, intubation & mechanical ventilation:
o indications:
 severe acidosis, PaCO2 > 60 mmHg or inability to increase PaO2
 deterioration of mental status, respiratory muscle fatigue

2. metabolic acidosis:
 low blood PH & low serum bicarbonate +/- respiratory alkalosis (compensation)
 causes:
- normal anion gap: diarrhea or renal tubular acidosis (RTA) (with high urine PH)
- high anion gap:
o internal: lactic acidosis, ketoacidosis (DM, alcohol), renal failure (uremia)
o external: intoxications (aspirin, methanol or ethylene glycol (give fomepizole))
 diagnosis: history & S&S (hyperventilation & decrease CO), calculation of ABG
 winter formula: expected PaCO2 = (1.5*HCO3) + 8 +/- 2
- if PaCO2 is in the normal range: simple metabolic acidosis
- if higher than expected: patient also has respiratory acidosis (serious)
 treatment: treat underlying cause, NaHCO3, +/- mechanical ventilation

3. respiratory alkalosis:
 high blood PH, low PaCO2 +/- renal compensation: (PH decrease by 0.08* & 0.03**)
- acute: HCO3 should decrease 1 mmol/L for every 10 mmHg decrease in PaCO2, *
- chronic: HCO3 should decrease 4 mmol/L for every 10 mmHg decline in PaCO2, **
 causes: anxiety, P embolism, hypoxia, pregnancy, drugs (aspirin toxicity), sepsis
 S&S: lightheadedness, dizziness, numbness, tetanus // complication: hypo PO4
 Tx: treat underlying cause, inhaled mixture containing CO2 or breath in paper bag

4. metabolic alkalosis:
 high blood PH, high serum HCO3, +/- high PaCO2 (compensation-hypoventilation)
 causes:
- saline sensitive (urine chloride < 10 mEq/L): vomiting, nasogastric tube, diuretics
- saline resistant (urine chloride > 20 mEq/L): 1ry hyperaldosteronism, Cushing`s
 diagnosis: hypokalemia, ABG, urine chloride
 Tx: treat underlying cause, NS + K (if saline sensitive), spironolactone (saline resistant)

5. how to assess the acid base imbalance:

 normal value:
- PH: 7.35 – 7.45 // Na: 135-145 // K: 3.5-5 // Cl: 98-106 // HCO3: 22-28
- PCO2: 35-45 mmHg // Po2: 80-100 mmHg
 1st step: look at the PH.
 2nd step: look @ HCO3 & PCO2 to determine primary disturbance; is it a metabolic or
respiratory?
 3rd step: assess the compensatory response:
- e.g. if the patient has a metabolic acidosis > assess the respiratory compensation.
o has the PCO2 decreased appropriately to compensate for the metabolic acidosis?
o normal compensatory response in metabolic acidosis is for the PCO2 to decrease by
1 to 1.5 mm Hg for each 1-mEq decrease in HCO3.
o Another method to assess compensation in a metabolic acidosis is Winters formula
 4th step: calculate the anion gap: Na – (Cl+HCO3) = normal anion gap is 8 to 12 mEq/L

 electrolytes imbalance:
1. hypercalcemia: (Ca > 10.5 mg/dL)
 severity: mild (10.5-12), moderate (12-14), severe (14-16)
 causes:
- endocrine: hyper-PTH, renal failure (2ry hyper-PTH), Paget disease, Addison disease
- malignancy: metastatic cancer (bone destruction), multiple myeloma, ectopic PTH
- drugs: thiazide diuretics, lithium, vitamin D intoxication
- others: sarcoidosis (increase Ca absorption in GI), familial hyper-Ca
 S&S:
- "stones" (nephrolithiasis & nephrocalcinosis), "bones" (bone pain, otitis fibrosa)
- "grunts & groans"(muscle pain, pancreatitis, PUD, gout), CVS (short QT, bradycardia)
- "psychiatric overtones"(confusion, depression, anorexia, sleep disturbances)
 diagnosis: PTH, Ca, Po4, TSH, vitamin D, IGF-1 (acromegaly), urinary cAMP
 treatment:
- increase urine excretion: NS fluids (1st step), loop diuretics (furosemide)
- inhibit bone resorption: bisphosphonates & calcitonin
- glucocorticoids (for multiple myeloma & vit D intoxication), hemodialysis (ESRD)

2. hypocalcemia:
 causes:
- hypoparathyroidism (1st cause), pancreatitis (fat saponification), hyperphosphatemia
- pseudo-hypoparathyroidism (high-PTH but resistant), hypo-Mg, drug (furosemide)
 S&S: “mostly asymptomatic, Rickets or osteomalacia”
- CNS: numbness, tetany (Chovestic sign (VII CN) & Trousseas sign), hyper-reflexia
- CVS: arrhythmia, prolong QT interval, hypotension // respiratory: bronchospasm
 diagnosis: Ca, PTH, Mg, pancreatic enzymes, PO4, vitamin D
 treatment:
- acute: IV Ca gluconate // long term: oral calcium carbonate & active Vit D (calcitriol)
- PTH deficiency: calcitriol + oral Ca +/- thiazide // dialysis Pt: Ca carbonate 3 times/wk