NEPHROLOGY (ME)

• most common cause of pre-renal AKI: Hypotension Gastritis, Vomiting and Diarrhea
• Most common cause of hospital acquired AKI: Acute renal Tubular Necrosis , or prolonged Pre-renal Statue .
• Two drugs causes AKI and How: NSAID: by Vasoconstriction of Afferent Blood flow , ACEI's : by Efferent Vasodilatation
• Pathophysilogy of AKI: Pre-renal , Renal and post renal
• Pre-renal causes of AKI Labs: Increase Bun+creatinine Ration >20% , Decrease FEna <1%
• Renal Lab: decreased BUN:creatinine Ration , FEna increases >2%
• Post renal causes : Obstruction from any site till the urethera
• Post renal Causes Labs: inccrease BUN:Creatinine Ratio
• Causes of Isolated High Bun reading : Upper GI bleeding.
• Acute Tubular Necrosis: Caused by : Drugs, toxins and prolonged pre-renal status
• Acute tubular necrosis Cassts: Muddy brown casts or Granular casts or Epithelial casts
• Urine Sodium in Acute tubular necrosis: High with FEna >2%
• Urine Microscopy:RBCs Cast or dysmorphic red cells indicates glomerulonephritis,Muddy brown or granular cast in ATN

  Hyaline cast in pre-renal causes

  WBC cast indicates infection or interstitial nephritis

  Fatty cast in nephrotic syndrome

  Waxy cast in chronic kidney disease
• Acute interstitial nephritis:- Triad of eosinophilia, fever and rash

  Presence of pyuria and eosinophiluria, hematouriea and protienurea

  Review patient’s medications list: penincillinm Cefuroxime and PPI+ NSAID

  • Eosinophiliuria DDx:- AIN and cholesterol emboli
• Cholestrol Emboli: Hx of recent PCI , comes presented by AKI+ Rash ( Levido reticularis)
• Rhabdomyolysis : Dark tea color urine with dipstick +ve for blood but no

  erythrocyte on UA

  Following heat exposure or crush injury

  High CK level

  • Treatment:- IV fluid
• Electrolytes in Rhabdomyolysis: Looks like Tumor lysis syndrome except there's Hypocalcemia
• Contrast induced Nephropathy :Increased serum creatinine within 24 to 48 hours following

  contrast exposure

  High risk for CIN:- recent AKI, eGFR < 30

  Only approved prophylaxis is IV 0.9 saline and use of isoosmolar

  or low osmolar contrast

  • No benefit of N-acetylcystine, dialysis post-contrast or sodium

  bicarbonate infusion
• Indication of acute renal replacement therapy:1- Refractory hyperkalemia

  2- Refractory fluid overload

  3- Refractory acidosis

  4- Uremic pericarditis or uremic encephalopathy

  5- Intoxication
• Post operative Patient presented with : Diffuse Discomfort , high creatinine and bun : Bladder catheterization
• Small kidneys on ultrasound suggest chronicity except in:-

  1. DM

  2- HIV

  3- Polycystic kidney disease

  4- Amyloidosis

  The kidneys will preserve its size

  N.B: most common cause of death in ESRD patient is

  cardiovascular diseases
• Diabetic Nephropathy: Protein > 3.5 Gm in diabetic patient

  Clinical diagnosis, absence of diabetic retinopathy make it unlikely

  cause of proteinuria

  Screen with albumin/creatinine ratio annually starting from:-

  At time of diagnosis for Type 2 DM

  5 years after diagnosis for Type 1 DM

  • Treatment:-

  BP and glucose control

  ACE inhibitors or ARBs
• If Diabetic patient have Proteinuria with micovascular invovment : no need for renal biopsy, DM+ no Microvascular Diseases = renal Biopsy
• Delaying progression of CKD:-

  1. BP control

  2- Glycemic control

  3- ACEi in case of proteinuria

  4- SGLT-2 inhibitors (Empagliflozin)

  5- Low protein diet (but not restricted and not in case of

  nephrotic syndrome)

  6- Sodium bicarbonate only in case of metabolic acidosis
• Anemia in chronic kidney disease:-

  Anemia of chronic inflammation, treated with SC Erythropoietin

  Iron deficiency anemia should be ruled out first and if present to be treated first

  Transferrin saturation < 20% + Ferritin < 100 à Iron supplement

  Transferrin saturation > 20% + Ferritin > 100 à SC Erythropoietin

  EPO in contraindicated in case of malignancy

  Target hemoglobin in CKD:- 10 – 11.5

  • One of side effects of EPO is hypertension
• Dialysis Disequilibrium Syndrome : Range of systemic and neurological symptoms occurs during

  dialysis especially in patients in whom dialysis is initially started

  Nausea, vomiting, headache, restlessness, seizure, coma

  Due to rapid shift of urea causing rapid lowering in serum

  osmolarity
• Calculating serum osmolarity: 2xNa+Glucose+BUN
• Best outpatient method for access to start hemodialysis: AV fistula m takes upto 6 months to maturate
• Nephrotic syndrome :

  protien in 24 hours urine : > 3.5 Gm

  Urine Casts: Fatty Casts

  Clinical symptoms: Generalized Edema , peri Orbital Edema

  Hyperlipidemia : Yes

  causes:

  1. Minimal change
  2. 2- Focal segmental Glomuronphritis
  3. membranous
  4. Diabetic Nephropathy
• Nephritic Syndrome:

  Protien 24 h in Urine: < 3.5 gm

  urine Casts: RBC casts

  Clinical symptoms: Hypertension

  Hyperlipidemia: no

  Diseases: Any other causes
• Nephoritc and Nephritic syndrome bothe need Renal Biopsy except Diabetic Nephropathy
• Minimal change disease:- most common in children, excellent response to steroid

  Membranous nephropathy:- associated with SLE, cancer (solid tumor or

  lymphoma), infections (HCV, HBV, syphilis or malaria), drugs like NSAIDs,

  strong association with thrombosis especially renal vein thrombosis, positive

  phospholipase A2 receptor antibody

  Focal segmental glomerlosclerosis:- Obese, black, HIV, Heroin use

  Diabetic nephropathy:- long-standing uncontrolled DM with presence of

  retinopathy
• To decrease protein in all nephrotic syndrome use

  ACEi except in minimal change disease treat the

  underlying cause with Prednisone
• IgA nephropathy presented within 3 days of URTI

  Post-infectious glomerulonephritis —> 10 days after a

  streptococcal throat infection or longer after a skin infection
• 90% of PSGN cases has low C3 and CH50 within first 2 weeks

  Returned to normal again within 4-8 weeks

  C4 is usually within normal
• Causes of glomerulonephritis associated with low serum complements:-

  • Post-infectious glomerulonephritis

  • Subacute bacterial infection, especially endocarditis

  • Systemic lupus erythematosus

  • Cryoglobulinemia

  • Membranoproliferative glomerulonephritis
• Alport syndrome

  Sensorineural hearing loss + Ocular findings (lenticonus)

  In presence of family Hx of ESRD

  Inherited defect in collagen Type 4
• 1. ACEI + ARBS are contraindicated together

  2- ACEI + ARBS during pregnancy are contraindicated

  3- ACEI is contraindicated in bilateral renal artery stenosis but can be used if unilateral

  4- HTN + DM = ACEI

  5- HTN + CKD = ACEI

  6- Beta blockers should not be used as a 1st line treatment except in case of CAD

  7- Avoid using CCB in patient with heart failure

  8- Labetalol is the best for HTN in pre-eclampsia

  Keywords for HTN in MCQs:-

  Calcium channel blocker
• Renal artery stenosis

  Fibromuscular dysplasia + early onset hypertension

  (especially in women) + Atherosclerotic stenosis +

  flash pulmonary edema + asymmetrical kidneys on

  US + rapid deterioration of RFT after using of ACEI

  + bruit near the umbilicus

  Next step: Doppler US

  Definitive diagnosis: CT angiography
• Drugs causing high K level:-

  β blockers

  ACE inhibitors

  ARBs

  Calcineurin inhibitors (cyclosporine)

  Spironolactone

  Eplerenone

  Amiloride

  Heparin

  NSAIDs