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Letuda’s Nephrology Note
Version 1.
Created and compiled by
Prithwiraj Maiti
R.G.Kar Medical College
Batch 2015
Table of contents
Content Page no.
Chronic kidney disease (ckd) 2
Anemia in ckd 11
Acute kidney injury (aki) 12
Acute tubular necrosis (atn) 13
Nephrotic syndrome 19
glomerulonephritis 22
Post-infectious gn 26
IgA NEPHROPATHY 27
HENOCH – SCHONLEIN PURPURA 27
MINIMAL CHANGE DISEASE 28
MEMBRANOUS NEPHROPATHY 29
UTI 30
VASCULITIS 33
WEGENER’S GRANULOMATOSIS 37
GOODPASTURE SYNDROME 37
CHURG-STRAUSS SYNDROME 38
LUPUS NEPHRITIS 39
Behçet's disease 40
Chronic kidney disease (CKD)
Definition:
Presence of any of the following for at least 3 months:
- Evidence of kidney damage with/ without reduced GFR OR
- GFR ≤60 ml/min/1.73 sq.mt body surface area.
Evidence of kidney damage:
- Biochemical abnormalities: Urea↑ Creatinine↑
- Urinary abnormalities: Proteinuria/ sediment/ cast
- Radiological evidence: Bilateral small kidneys
- Histopathological abnormalities.
Stages of CKD:
Stage GFR (Normal: ≥90) Description 1 Evidence of kidney damage +Ve when GFR ≥
Minor kidney damage
2 60-89 Mild 3 30-59 Moderate 4 15-29 Severe 5 <15 Kidney failure/ end stage renal disease*
*It is a condition where without renal replacement therapy (dialysis/ renal transplantation), patient will not survive.
Azotemia and uremia
Azotemia : Accumulation of nitrogenous substance in the blood due to defective renal clearance.
Uremia : Clinical manifestations due to azotemic condition.
Pathophysiological effects of CKD:
Effects of CKD on bone:
Effect on bone mineralization
- De-mineralization
- Osteitis fibrosa cystica.
Pathophysiological effects of CKD
A
Azotemia (toxic N substances)
Constitutional symptoms
Encephalopathy
Pericarditis
Peripheral neuropathy
B
↑BP
Accelerated atherosclerosis
Na+/ water retension
Bone
Effect on bone metabolism
Renal osteodystrophy
Blood
C
Circulatory changes
Renal osteodystrophy
Effect of CKD on blood picture:
- ↓Erythropoietin synthesis -- Anemia
- ↑Toxins-- Platelet dysfunction.
Circulatory effect:
CKD
↓PO 4 - clearance
↑Serum PO 4 - level
↓1,25 (OH)2 cholecalciferol
↓Calcium absorption
↓Serum Ca++ (Hypocalcemia)
↑PTH secretion
Secondary hyperparathyroidism
Water retention
Volume overload
Congestion
Systemic venous congestion
Pulmonary congestion
Preliminary investigations
A. Blood biochemistry : Urea creatinine: ↑ Na+: Normal/ ↓ (due to dilutional hyponatremia) K+: Normal/ ↑ Ca++: Normal/ ↓ PO 4 -: Normal/ ↑
ABG: pH↓ (due to ↓HCO 3 -) Vitamin D level: Normal/ ↓ PTH level: Normal/ ↑ Uric acid: Normal/ ↑ Hb level: Normal/ ↓
Special note: Blood glucose in diabetic patients: Often glucose control becomes better/ patient may develop recurrent hypoglycemia due to delayed excretion of insulin which in turn prolongs half- life of insulin. Therefore in diabetic patients, once CKD develops, dose of medications often needs to be decreased.
B. Calculating creatinine clearance:
𝐶𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒 𝑐𝑙𝑒𝑎𝑟𝑎𝑛𝑐𝑒
=
(140 − 𝑃𝑎𝑡𝑖𝑒𝑛𝑡′𝑠 𝑎𝑔𝑒) × 𝑃𝑎𝑡𝑖𝑒𝑛𝑡′𝑠 𝑏𝑜𝑑𝑦 𝑤𝑒𝑖𝑔ℎ𝑡 (𝑖𝑛 𝑘𝑔)
𝑆𝑒𝑟𝑢𝑚 𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒 𝑙𝑒𝑣𝑒𝑙 (𝑖𝑛 𝑚𝑔/𝑑𝑙) × 72 = 𝑥
For females, 𝐶𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒 𝑐𝑙𝑒𝑎𝑟𝑎𝑛𝑐𝑒 = 𝑥 × 0.
C. Urine (microscopic examination): To look for biochemical abnormalities: Proteinuria Any cast (particularly RBC case, tubular cast): May give an idea about the underlying disorder.
24 hour urine for albumin: creatinine/ microalbumin: creatinine ratio.
D. Kidney-ureter-bladder (KUB) USG:
Bilateral small kidneys (seen in CKD) Unilateral small kidney (seen in renal artery stenosis).
E. Chest X-Ray, ECG, Echo: To look for any cardiac pathology.
F. Renal biopsy: In selected cases only: confirms the underlying type of kidney disease: which in most cases are: unexplained glomerulonephritis and nephrotic syndrome.
G. Relevant investigation(s) to detect the cause.
Treatment General treatment
R:
- R egular monitoring of urine output: particularly in significant CKD
- R egular monitoring of volume status, i.e. regular monitoring of body weight
- R egular monitoring of blood biochemistry.
E:
Treatment of the underlying e tiology.
N:
Maintenance of n utrition: Dietary modification Fluid and salt restriction Dietary protein restriction In presence of associated DM: Restriction of carbohydrate Restriction of K+: o Parboiling of rice (to discard water after boiling) o Avoid juicy food. Avoid beverages (as they are rich in phosphates).
I:
Infection: Treat with appropriately adjusted dose of antibiotics.
L:
Loss of blood due to associated coagulopathy: Treat with blood transfusion.
U:
Treat uremic encephalopathy Treat uremic pericarditis
R:
Treatment of r enal osteodystrophy, if present:
The underlying biochemical abnormalities are: ↑ PO 4 - , ↓Vit-D, ↓Ca, ↑PTH.
↑ PO 4 -:
- PO 4 - restriction
- PO 4 - binding agents: o Calcium agents (Ca-carbonate/ Ca-acetate) o Non-calcium agents (Sevelamer). ↓Vit-D: Cholecalciferol/ Calcitriol. ↓Ca: Ca-salts ↑PTH: Calcimimetics: Cinacalcet.
E:
- Treat any e lectrolyte imbalance: Electrolyte imbalance Treatment ↓Na+ Fluid restriction
Diuretics ↑K+ Restriction of dietary K+ intake Regular monitoring of serum level
Severe ↑K+
IV Ca-gluconate Counteract cardiac toxicity IV Dextrose + Insulin OR Nebulized salbutamol
Shifts extracellular K+ to intracellular compartment
Dialysis
- Treatment of e nd stage renal disease: a. Dialysis: o Hemodialysis o Peritoneal dialysis. b. Kidney transplantation.
Anemia in CKD
Pathogenesis/ mechanism:
- ↓Erythropoietin (EPO) synthesis
- Marrow suppression by azotemic toxins
- ↓RBC life span
- Coexistent iron deficiency
- ↑Loss of folic acid (particularly in patients on dialysis)
- Blood loss due to coagulopathy.
Clinical features:
A. Asymptomatic B. If symptomatic: A. Anemic look B. Breathlessness C. Cardiac palpitation D. Dizziness E. Exercise intolerance F. Fatigue.
Causes of AKI:
- Pre-renal causes : Hemorrhagic shock (massive bleeding) Hypovolemic shock (severe dehydration) Cardiogenic shock (MI, acute LVF, acute RVF) Fluid sequestration (septicemic shock, acute pancreatitis) Septicemic shock (abnormal peripheral vasodilatation) Severe burn (↑ Insensible loss).
- Intrinsic renal causes : I. Acute glomerular diseases: RPGN MPGN IgA nephropathy. II. Acute tubular necrosis: Ischemic (pre-renal causes) Toxins (endogenous and exogenous). III. Acute interstitial nephritis: Iatrogenic (β-lactam antibiotics) Idiopathic Infection (CMV). IV. Renal vasculitis: Microangiopathic hemolytic anemia DIC.
- Post-renal causes : An obstructive uropathy can cause AKI, particularly if there is single functioning kidney: Calculus Carcinoma Bladder outlet obstruction Structure.
Acute tubular necrosis (ATN)
Acute tubular damage leading to acute malfunctioning of kidney.
Causes:
Pathophysiology:
ATN
Ischemic causes
Pre-renal causes
Toxins
Endogenous toxins
Hb : Mismatched blood transfusion
Myoglobin : Crush injury/ rhabdomyolysis
Urate crystals : Hyperuricemia
Exogenous toxins
Drugs
Aminoglycosides
Radiocontrast dye
Snake bite Complicated malaria
AKI
Azotemia
Uremic
Constitutional symptoms
Encephalopathy
Pericarditis
BP
↓BP due to underlying pre-renal causes
Blood chemistry
Urea creatinine↑
Na+: N/↑/↓
K+: ↑
Metabolic acidosis
Circulatory
Hypovolemia (due to underlying pre- renal causes)
Hypervolemia (due to impaired fluid excretion)
Pulmonary congestion
Systemic congestion
Stages of progression of AKI:
Stage Description Stage of progression Due to sudden assault on kidney, GFR abruptly decreases which in turn leads to ↓urinary output and accumulation of excessive salt, water and toxins Stage of maintenance Falling GFR reaches its lowest limit leading to a full blown picture of AKI Stage of recovery With treatment, kidney starts to regain its function. Often in this stage, recovery of tubular function (salt and water retention) lags behind recovery of glomerular function. Patient goes into polyuric phase temporarily.
Investigations of AKI:
- Full blood count
- Urea creatinine: ↑
𝐵𝑈𝑁 =
Is strongly suggestive of ATN.
𝐵𝑈𝑁 𝐶𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒
May be found in both pre-renal/ post-renal causes of AKI.
- Electrolyte: o Na+: Variable (depends upon the degree of fluid and solute loss) o K+: Normal/ ↑ (hypokalemia may occur in diarrhea/ overdiuresis).
- Blood gas analysis:
Metabolic Acidosis (^) vasodilationPeripheral BP↑ Cardiac arrhythmia
- Urine routine examination/ microscopic examination: Often gives vital clue of underlying causes. Ex.: Tubular cast is suggestive of ATN RBC cast ± Dysmorphic RBCs is suggestive of GN.
- KUB-USG: To look for any obstructive uropathy.
- Chest X Ray: To look for any pulmonary edema.
- ECG: To rule out any cardiac pathology due to hyperkalemia.
- Echocardiogram: IVC collapsibility/ fullness indicates volume overload and volume overloaded state respectively.
- Investigation(s) to assess the underlying disease. If cause is not obvious, patients are often investigated for: Underlying glomerulonephritis: Autoantibody markers Endogenous toxins: Serum uric acid, Serum + urinary protein electrophoresis Renal biopsy. Treatment
General treatment:
- Absolute bed rest till patient is stable
- Regular monitoring of volume status: a. Urine output [intake-output chart] b. Central venous pressure measurement c. Echocardiogram: Status of IVC. C. Treatment of the etiology D. Nutrition: Protein and K+ restriction. E. Avoid all nephrotoxic drugs F. Adjust dosage of dugs according to creatinine clearance
iii. Significant acidosis iv. Severe hyperkalemia.
Nephrotic syndrome
Introduction:
It is a condition characterized by:
- Heavy proteinuria (>3 gm/24 hr)
- Hypoalbuminemia
- Hyperlipidemia.
Causes:
Physiological effects:
- Hypoalbuminemia : Due to increased tubular permeability causing heavy proteinuria.
Glomerular causes
Primary
Minimal change disease
MPGN
FSGS
MPGN
Secondary
Diabetes Amyloidosis Drugs
Gold
Penicillamine
HIV nephropathy
- Hyperlipidemia : I. Accelerated lipid synthesis II. Loss of lipid metabolizing protein.
- Hypercoagulability : Due to loss of circulating anticoagulant antithrombin.
- Hypervolemia:
- Hormonal disturbance: Due to loss of hormone binding proteins, causing: Hypothyroidism Hypovitaminosis-D.
- Hypo-gamma-globulin-emia: It makes the patient prone to infection.
Clinical features:
Symptoms:
Progressive swelling of body Recurrent infection particularly in children Patient may develop unprovoked DVT; particularly renal vascular thrombosis , causing acute loin pain ± hematuria.
Signs:
Edema: ++
Hypoalbuminemia Colloidal osmotic pressure ↓ Fluid leakage
Intravascular volume depletion
Renal hypoperfusion
↑ Activity of RAS system
Secondary hyperaldosteronism
Na+ and water retention Hypervolemia
