Nephrology
Acute kidney injury (AKI)
➢ A reduction in renal function following an insult to the kidneys which occur over hours to days
Causes
➢ Prerenal ⟶ Ischemia ATN (acute tubular necrosis)
• Most common renal cause of AKI
• Hypovolemia secondary to diarrhea/vomiting
• Occurs after a prolonged ischemic event
• Renal artery stenosis (e.g. massive hemorrhage, hypotensive
➢ Intrinsic shock) with increased creatinine
• AGN • There may be a history of nephrotoxins
• Acute tubular necrosis (ATN) interstitial nephritis (allergic)
• Acute interstitial nephritis (AIN) ➢ Allergy + hematuria
• Rhabdomyolysis
• Tumor lysis syndrome (after killing large amount of tumor cells)
➢ Postrenal
• Kidney stone in ureter or bladder Drugs that are safe in AKI:
• Benign prostatic hyperplasia (BPH) - Paracetamol
- Warfarin
• External compression of the ureter
- Statins
Risk factors - Aspirin
• CKD - Clopidogrel
• Other organ failures - B-blockers
• Hx of AKI
• Nephrotoxic drugs (e.g. NSAIDs, aminoglycosides, ACE inhibitors & diuretics) ⟶ [DAMN]
• Usage of iodinated contrast in the past week
• >56 years old
Features
➢ Maybe asymptomatic until renal failure progresses
• Oliguria (<0.5 ml/kg/hour)
• Fluid over load ⟶ pulmonary and peripheral edema
• ↑ K+ ⟶ Arrythmias
• ↑ Urea & creatinine ⟶ pericarditis or encephalopathy
Chronic kidney disease (CKD)
➢ CKD results in decreased activity of 1-alpha
Symptoms hydroxylase which is responsible for the
• Usually asymptomatic, may be discovered by a chance conversion of 25-hydroxyvitamin D to its active
• Specific symptoms in severe CKD form 1,25-dihydroxyvitamin D (especially when
GFR is <30 mL/min) ⟶ low Ca absorption ⟶
- Peripheral edema
high parathyroid hormone
- Pruritis ➢ Findings in CKD
- Nausea, vomiting, fatigue • Small kidneys (<9cm)
- Sexual dysfunction • Anemia
Signs • Low Ca
• High PO4
• Skin pigmentation
• Pallor (due to anemia of chronic disease)
➢ The only definite sign of CKD is previous blood results showing high creatinine/low GFR
Management
• ACEI (e.g. Lisinopril) or ARB in all ethnic groups with CKD and HTN
- ACR (albumin creatinine ratio) ≥ 70
- ACR ≥ 30 + HTN • ACEIs are contraindicated in renal artery
stenosis and severe hyperkalemia
- ACR ≥ 3 + Diabetic
PLABverse - 1
, Nephrology
NephrOtic syndrome ⟶ loss of a lot of prOtein
➢ 1ry causes (80%)
• Children, young adults ⟶ Minimal change disease
• Elder adults ⟶ Membranous GN, minimal change nephropathy or Focal & segmental glomerulosclerosis
➢ 2ry causes
• SLE (comes 3rd as in the most common causes in adults)
• Hepatitis B & C, HIV
• DM, Amyloidosis ➢ A child with LL edema ⟶ order 24hr urine protein ⟶
Triad order serum albumin, if confirmed nephrotic $ ⟶
1. Proteinuria (≥3 gm/24hr) refer to a nephrologist
2. Hypoalbuminemia (≤ 30g/L) ➢ Definitive investigation is Renal biopsy
- Minimal change disease ⟶ fusion of podocytes
3. Edema (pre-orbital)
Complications
• Renal vein thrombosis (due to loss of anti-coagulation factors in urine e.g. Antithrombin III)
- Sudden left loin pain, hematuria & sudden swelling of the left testis
• Infections (due to loss of immunoglobulin proteins in urine)
• Na+ retention (due to 2ry hyperaldosteronism as a result of low renal perfusion)
• Hypercholesterolemia (due to non-specific increase in cholesterol synthesis)
Management
• Diet: Fluid restriction, low salt and sufficient protein
• Drugs: steroids (if resistance ⟶ cyclophosphamide) & diuretics
Nephritic syndrome ⟶ loss of a lot of blood
➢ Hematuria (microscopic or macroscopic) + red cell cast
➢ Proteinuria (++)
➢ Hypertension (mild) ➢ Goodpasture’s treated with plasmapheresis
➢ Low urine output (<300 ml/day) and immunosuppressants
Causes
• Post-streptococcal GN ⟶ appear after 1-2 weeks after URTIs
• IgA nephropathy (Berger’s disease) ⟶ appears after 1-2 days after URTIs
• Rabidly progressive glomerulonephritis
o Goodpasture’s $ (Anti-GBM antibodies)
o Vasculitis disorder: Wegener’s granulomatosis (C-ANCA), Churg Strauss disease (P-ANCA)
• Membranoproliferative GN
• Henoch-Schoenlein purpura ⟶ PAAN
ADPKD
Hematuria + HTN
- US
Goodpasture’s $
Hematuria + Hemoptysis - Anti-GBM antibodies
- Kidney or lung biopsy
Wegener’s granulomatosis
Hematuria + Hemoptysis + Nasal/sinus problems
- C-ANCA
Hematuria + Jaundice Alpha 1-antitrypsin deficiency
PLABverse - 2
Acute kidney injury (AKI)
➢ A reduction in renal function following an insult to the kidneys which occur over hours to days
Causes
➢ Prerenal ⟶ Ischemia ATN (acute tubular necrosis)
• Most common renal cause of AKI
• Hypovolemia secondary to diarrhea/vomiting
• Occurs after a prolonged ischemic event
• Renal artery stenosis (e.g. massive hemorrhage, hypotensive
➢ Intrinsic shock) with increased creatinine
• AGN • There may be a history of nephrotoxins
• Acute tubular necrosis (ATN) interstitial nephritis (allergic)
• Acute interstitial nephritis (AIN) ➢ Allergy + hematuria
• Rhabdomyolysis
• Tumor lysis syndrome (after killing large amount of tumor cells)
➢ Postrenal
• Kidney stone in ureter or bladder Drugs that are safe in AKI:
• Benign prostatic hyperplasia (BPH) - Paracetamol
- Warfarin
• External compression of the ureter
- Statins
Risk factors - Aspirin
• CKD - Clopidogrel
• Other organ failures - B-blockers
• Hx of AKI
• Nephrotoxic drugs (e.g. NSAIDs, aminoglycosides, ACE inhibitors & diuretics) ⟶ [DAMN]
• Usage of iodinated contrast in the past week
• >56 years old
Features
➢ Maybe asymptomatic until renal failure progresses
• Oliguria (<0.5 ml/kg/hour)
• Fluid over load ⟶ pulmonary and peripheral edema
• ↑ K+ ⟶ Arrythmias
• ↑ Urea & creatinine ⟶ pericarditis or encephalopathy
Chronic kidney disease (CKD)
➢ CKD results in decreased activity of 1-alpha
Symptoms hydroxylase which is responsible for the
• Usually asymptomatic, may be discovered by a chance conversion of 25-hydroxyvitamin D to its active
• Specific symptoms in severe CKD form 1,25-dihydroxyvitamin D (especially when
GFR is <30 mL/min) ⟶ low Ca absorption ⟶
- Peripheral edema
high parathyroid hormone
- Pruritis ➢ Findings in CKD
- Nausea, vomiting, fatigue • Small kidneys (<9cm)
- Sexual dysfunction • Anemia
Signs • Low Ca
• High PO4
• Skin pigmentation
• Pallor (due to anemia of chronic disease)
➢ The only definite sign of CKD is previous blood results showing high creatinine/low GFR
Management
• ACEI (e.g. Lisinopril) or ARB in all ethnic groups with CKD and HTN
- ACR (albumin creatinine ratio) ≥ 70
- ACR ≥ 30 + HTN • ACEIs are contraindicated in renal artery
stenosis and severe hyperkalemia
- ACR ≥ 3 + Diabetic
PLABverse - 1
, Nephrology
NephrOtic syndrome ⟶ loss of a lot of prOtein
➢ 1ry causes (80%)
• Children, young adults ⟶ Minimal change disease
• Elder adults ⟶ Membranous GN, minimal change nephropathy or Focal & segmental glomerulosclerosis
➢ 2ry causes
• SLE (comes 3rd as in the most common causes in adults)
• Hepatitis B & C, HIV
• DM, Amyloidosis ➢ A child with LL edema ⟶ order 24hr urine protein ⟶
Triad order serum albumin, if confirmed nephrotic $ ⟶
1. Proteinuria (≥3 gm/24hr) refer to a nephrologist
2. Hypoalbuminemia (≤ 30g/L) ➢ Definitive investigation is Renal biopsy
- Minimal change disease ⟶ fusion of podocytes
3. Edema (pre-orbital)
Complications
• Renal vein thrombosis (due to loss of anti-coagulation factors in urine e.g. Antithrombin III)
- Sudden left loin pain, hematuria & sudden swelling of the left testis
• Infections (due to loss of immunoglobulin proteins in urine)
• Na+ retention (due to 2ry hyperaldosteronism as a result of low renal perfusion)
• Hypercholesterolemia (due to non-specific increase in cholesterol synthesis)
Management
• Diet: Fluid restriction, low salt and sufficient protein
• Drugs: steroids (if resistance ⟶ cyclophosphamide) & diuretics
Nephritic syndrome ⟶ loss of a lot of blood
➢ Hematuria (microscopic or macroscopic) + red cell cast
➢ Proteinuria (++)
➢ Hypertension (mild) ➢ Goodpasture’s treated with plasmapheresis
➢ Low urine output (<300 ml/day) and immunosuppressants
Causes
• Post-streptococcal GN ⟶ appear after 1-2 weeks after URTIs
• IgA nephropathy (Berger’s disease) ⟶ appears after 1-2 days after URTIs
• Rabidly progressive glomerulonephritis
o Goodpasture’s $ (Anti-GBM antibodies)
o Vasculitis disorder: Wegener’s granulomatosis (C-ANCA), Churg Strauss disease (P-ANCA)
• Membranoproliferative GN
• Henoch-Schoenlein purpura ⟶ PAAN
ADPKD
Hematuria + HTN
- US
Goodpasture’s $
Hematuria + Hemoptysis - Anti-GBM antibodies
- Kidney or lung biopsy
Wegener’s granulomatosis
Hematuria + Hemoptysis + Nasal/sinus problems
- C-ANCA
Hematuria + Jaundice Alpha 1-antitrypsin deficiency
PLABverse - 2
