1
Q
Define CKD
A
Severe reduction in nephron mass over time (at least 3 months, other wise AKI) resulting in uraemia
2
Q
Name 8 causes of CKD
A
- Glomerulonephritis
- DM (cause glomerulosclerosis over time) !!! (Most common)
- Toxic nephropathies:tobacco, traditional medicine alcohol
- Polycystic kidney disease
- Systemic vascular disease
- Hypertensive nephrosclerosis !!!
- Autoimmune disorders: SLE, rheum arthritis, HIV
- Analgesic nephropathy: NSAIDs
HAT PAD: Hypertensive, autoimmune, toxins, analgesic, poly cystic kidneys, diabetes
3
Q
Common symptoms CKD (4)
A
Confusion - coma/ death (encephalopathy)
Muscle cramps
Bleeding
Loss appetite, nausea
4
Q
Skin signs CKD (3)
A
Subcut nodules: Calcium phosphate deposits
Scratch marks (pruritis)
Pallor (anaemia)
5
Q
Hand signs CKD (3)
A
Leuconychia
Asterixis
Uraemic frost
6
Q
Heart signs CKD(2)
A
- Pericarditis due to uraemia
- Arrhythmia due to hyperk
7
Q
Vital sign CKD
A
Increased BP
8
Q
Definition of nephrotic syndrome (4 points)
A
- Proteinuria >3,5 g per 24h (other features caused by this )
- hypoalbuminaemia <25-30g/L
- Edema
- Hyperlipidaemia
Other: urine protein:creatinine >0.2g/mmol
9
Q
Causes of nephrotic syndrome (5)
A
Primary
Glomerulonephritis (minimal change gn in children, membranous gn most common in adults, mesangiocapillary , proliferative) or glomerulosclerosis (focal segmental) = 80 %
Secondary
• drugs: penicillamine, lithium, ampicillin, bisphosphonates, NSAIDs, allergies
• systemic disease!: SLE,DM, amyloidosis
• malignancy
• infections: hepatitis, ie, malaria, HIV
10
Q
Definition of nephritic syndrome (4)
A
PHAROH
- Haematuria
- only mild to moderate Proteinuria <3.5g per 24h
- Azotemia (increased urea and creatinine)
- Oliguria
- red cell casts
- HT
11
Q
Name 7 complications of CKD
A
A WET BED
- acidosis (metabolic): inability kidneys to excrete acid
- water: pulmonary oedema
- erythropoiesis: anaemia of chronic disease; bleeding due to uraemic coagulopathy
- toxins: uraemic encephalopathy
- bp: cardiovascular disease (due to combination of bp, salt + water over load,accelerated atherosclerosis)
- electrolytes: hyperkalaemia, hyper P, hypo Ca
- D vitamin: ckd-bmd (due to increased secretion PTH [ 2° hyperparathyroid ] due to impaired renal hydroxylation of vit D and renal P retention )
12
Q
Name 3 complications nephrotic syndrome
A
- Infections: loss immunoglobulins in urine. Prone to cellulitis, strep, spontaneous bacterial cellulitis
- thromboembolism: eg DVT /pe, renal vein thrombosis. Due to increased clotting factors and platelet abnormalities
- hyperlipidaemia: due to hepatic lipoprotein synthesis in response to low oncotic pressure
13
Q
Treatment nephrotic syndrome? (5)
A
- Monitor UCE, bp, fluid balance, weight regularly. Treat underlying cause.
- restrict salt. Take in protein normally
- diuretics: furosemide with or without spironolactore. Aim 1 kg/day loss
- chronic nephrotic: ace -I renoprotective - reduce proteinuria and slow progression of renal impairment. Some also advocate A2A (adenosine A2A R agonist - decrease inflammation and prevent fibrosis)
- treat infections promptly (pneumococcal vaccines recommended) , prophylactic heparin if immobile, treat HPT , persisting hyperlipid and other risk factors.
14
Q
Name 5 indications for acute dialysis
A
Aeiou
- Acidosis severe metabolic: ph < 7,2 or base excess <10
- electrolytes: persistent hyper k >7
- intoxication: istumbled ( INH, salicylates, theophylline, uraemia, methanol, barbiturates, lithium, ethylene glycol aka antifreeze, dabigatran )
- overload: refractory pulmonary oedema,,
- uraemia: encephalopathy, uraemic pericarditis
15
Q
Approach to causes acute kidney injury? (10)
A
Prerenal = hypoperfusion
- hypovolaemia
- sepsis
- drugs
- hyper calcaemia
Renal
- vascular
- glomerular
- interstitial
- tubular
- hepatorenal syndrome
Postrenal (especially if solitary kidney)
- neurogenic
- anatomic
16
Q
Name 4 causes prerenal AKI
A
Due to kidney Hypoperfusion
- Hypovolaemia
→ absolute: haemorrhage, gi loss, skin loss, renal loss, renal artery stenosis
→ effective: low cardiac output (cardiac failure), cirrhosis, sepsis, 3rd space loss - Sepsis → systemic vasodilation
- Drugs: NSAIDs (constrict Afferent arteriole ), ace - I /arbs (inhibits vasoconstriction of efferent arteriole), calcineurin inhibitors (cyclosporine)
- Hypercalcaemia
17
Q
Name 10 renal causes AKI
A
Tubular
- acute tubular necrosis (50% mortality)
→ ischaemiA (due to prerenal causes)
→ nephrotoxins: drugs (aminoglycosides, amphotericin b, tetracyclines), contrast, uric acid crystals, haemoglobinura in rhabdomyolysis, myeloma
Vascular
- vasculitis
- malignant hypertension
- cholesterol emboli
- haemolytic uraemiC syndrome
- thrombotic thrombocytopeniC purpura TTP
Glomerular
- glomerulonephritis
Interstitial
- acute interstitial nephritis
Hepatorenal syndrome
18
Q
Name 6 postrenal causes AKI
A
Neurogenic urinary tract obstruction
- multiple sclerosis
- spinal cord lesion
- peripheral neuropathy
Anatomic
- ureter: stones
- bladder: tumour
- urethra: posterior urethral valve, BPH
19
Q
Name 4 clues to prerenal etiology of AKI
A
- Clinical: decreased bp, high hr, orthostatic hr /bp changes
- urea x 20 = more than the creatinine (urea increase more than creat)
- hyaline casts
- urine Na < 10-20 , fractional excretion of Na <1 %
- urine osmolality > 500
Why? Urine is concentrated and sodium is reabsorbed by working tubular cells.
20
Q
Name 5 clues to renal etiology of AKI
A
- Urinalysis positive for casts (tubular = pigmented granular, interstitial = WBC, glomerular = rbc)
- systemic features, anaemia , ht, mild-moderate ECF volume overload
- thrombocytopenia
- urine Na > 40 , fractional Na excretion > 2% in ATN
- urine osmolality < 350 in ATN
Why? Urine not concentrated and sodium not reabsorbed by sick tubules
21
Q
Name 5 clues to postrenal aetiology of AKI
A
- Known solitary kidney
- older man (bph)
- recent retroperitoneal surgery
- signs urinary tract obstruction: anuria, palpable bladder
- ultrasound shows hydronephrosis
22
Q
Name the 4 phases AKI
A
- Initiating event ( hours to days)
- oliguric/anuric phase (1-3 weeks) (fluid retention, hyperk)
- polyuric/ diuretic phase (2 weeks) (dehydration, hypo Na, hypok)
- recovery phase (months years)
23
Q
Name complications renal failure
A
Mad hunger
- metabolic acidosis
- dyslipidaemiA
- high potassium
- uraemia
- Na/H2O retention
- growth retardation
- erythropoietin failure (anaemia)
- renal osteodystrophy
24
Q
Diagnostic criteria AKI? (3)
A
Akin/kdigo criteria
Urine output < 0,5 ml /kg/hour for > 6h
Or
Increase serum creatinine 0,3 mg/ dL or more within 48 hours
Or
Increase serum creatinine 50% or more within 7 days
25
Staging criteria AKI? (5)
Rifle criteria
- Risk (stage 1): increase serum creat 1,5 x baseline or urine output < 0,5 ml/kg/hour for 6-12h
- injury (stage 2 ): increase serum creat 2 x baseline or urine output < 0,5 ml/kg/hour for 12-24 h
- failure (stage 3 ): increase serum creat 3 x baseline or urine output < 0, 3 ml/kg/hour for > 24h or anuria >12h or increase serum creat by > 0,5 - > 4.0 mg/dl or initiation renal replacement therapy
- loss: RRT > 4 weeks
- end stage: > 3 months
26
Treatment AKI? (6)
General
- Treat underlying cause and stop nephrotoxic drugs
- correct volume depletion with normal saline
- diet: normal calorie intake, protein 0,5 kg/day
Treat complications
- hyperkalaemia: iv calcium gluconate (cardioprotective), iv insulin and glucose to promote uptake, salbutamol nebuliser, calcium resonium to bind K in gut.
- pulmonary oedema: sit up, high flow oxygen. Venous vasodilator eg morphine. Furosemide.
- bleeding: FFP and platelets as needed
- Acute dialysis if indicated
27
Define ckd
Abnormality of kidney structure/function for at least 3 months with GFR < 60 or markers of kidney damage (proteinuria, haematuria, raised creat, small kidneys on u/s, biopsy abnorms)
28
CKD staging? (5)
Kdigo staging
- stage 1: GFR 90 or more (normal) with other evidence kidney damage
- 2: GFR 60 - 89 + other evidence kidney damage
- 3: GFR 30 - 59 + or - other evidence kidney damage
→ 3a: GFR 45 - 59
→ 36: 30 -44
- 4: GFR 15 - 29 + or - other evidence kidney damage
- 5: < 15. End stage renal disease.
29
Causes CKD? (8)
Prenenal
- dm!
- ht!
- SLE, hepatitis b/c
Renal
- glomerulonephritis!
- renovascular disease!
- pyelonephritis!
- polycystic kidneys!
- interstitial nephritis!
- nephrocalcinosis (ageing)
- Analgesic nephropathy
30
How manage CkD complications? (10)
Nephron
- Nitrogen: low nitrogen diet. Na restriction.
- Electrolytes: monitor K. Restrict in diet. If hyper K, kexelate (polystyrene sulfonate) 15g 6-24hrly
- ph: metabolic acidosis
- hypertension: ace-i or A2A can decrease rate of loss of renal function even if bp normal.; Hyperlipid: Statins
- RBCs: manage anaemia with erythropoietin; Restless legs: clonazepam /Gabapentin
- osteodystrophy: give Ca between meals to increase ca, and Ca with meals to bind and decrease PO4. Restrict dietary PO4 (milk, cheese, eggs). Supplement Vit D; Oedema: loop diuretics
- nephrotoxins: avoid eg ASA, gentamicin and adjust doses of renally excreted medications.
All must get pneumococcal vaccine every 5 years, influenza annually, hep B to susceptible
31
Name 3 causes nephritic syndrome
Infections
- post-streptococcal glomerulonephritis (type 3 hypersensitivity reaction, + anti-aso, anti - DNase, decrease C3)
Immune complex mediated
- IgA nephropathy/Berger's disease
- rapidly progressing glomerulonephritis (causes = goodpasture syndrome, SLE nephritis)
- membranoproliferative glomerulonephritis (type 1 = ig mediated; 2 = C3 )
Vascular
- small vessel vasculitis (henoch schonlein purport, Churgg Strauss syndrome )
32
Calcium, phosphate, vitamin d, PTH levels in renal osteodystrophy?
Calcium + vitamin D low
Phosphate, PTH high
33
Investigation for nephritic and nephrotic syndrome?
Biopsy
34
What is the hallmark of glomerular injury/disease?
Proteinuria
35
Name 4 causes acute interstitial nephritis
Characterised by electrolyte abnormalities, moderate proteinuria, renal impairment
- drug allergic: penicillins, NSAIDs, PPI, mesalizine ( aminosalicylate used for IBD )
- immune
- infection: TB, acute bacterial pyelonephritis
- toxic: mushrooms
36
Name 6 common clinical features polycystic kidney disease
- Vague discomfort in loin/abdomen
- acute loin pain/ renal colic due to haemorrhage into cyst
- ht
- haematuria,, with little/no proteinuria
- UTI
- renal failure
37
Name 6 presentations and clinical features renal artery stenosis
- Severe, recent onset, refractory ht
- kidneys asymmetrical
- flash pulmonary oedema occurs repeatedly, especially if bilateral
- peripheral vascular disease
- renal impairment, especially if bilateral
- renal function deterioration on ace -i/ arb
38
Define haemolytic uraemic syndrome
Type of thrombotic microangiopathy that predominantly affects renal microcirculation, with involvement of other organs (including brain ) in severe cases
39
Name 3 thrombotic microangiopathies associated with acute renal damage
- Haemolytic uraemic syndrome
- TTP
- Dic
40
Cause haemolytic uraemic syndrome
Infections with organisms that produce enterotoxins : E. coli, shigella dysenteriae
41
Complication untreated pre renal AKI?
Acute tubular necrosis
42
Name 5 options renal replacement therapy
- Haemodialysis
- haemofiltration
- haemodiafiltration
- peritoneal dialysis
- renal transplant
43
Most common type renal stone?
Calcium oxalate
