Nephrology & Urology Flashcards
Causes of renal disease following URTI
IgA nephropathy
Post-streptococcal glomerulonephritis
Raised anti-streptolysin O titre - meaning
it is likely that the person tested has had a recent strep infection.
ASO titers that are initially high and then decline suggest that an infection has occurred and may be resolving.
What is post-streptococcal glomerulonephritis
Occurs 1 – 3 weeks after a β-haemolytic streptococcus infection, such as tonsillitis
Immune complexes made up of streptococcal antigens, antibodies and complement proteins get stuck in the glomeruli of the kidney and cause inflammation –> AKI
What is IgA Nephropathy?
AKA Berger’s disease. Related to Henoch-Schonlein Purpura (IgA vasculitis)
IgA deposits in the nephrons of the kidney causes inflammation (nephritis).
Two most common causes of nephritis in children
post-streptococcal glomerulonephritis IgA nephropathy (Berger’s disease)
Similarities and differences between IgA Nephropathy and post-streptococcal glomerulonephritis
Similarities:
- Recent URTI
- Haematuria
Differences:
- PSGN develops 1-2 weeks after URTI.
- IgA nephropathy develops 1-2 days after URTI
Testicular problem associated with mumps
Orchitis
Indications for dialysis in AKI
Life threatining, refactory AKI with complications:
I) Severe hyperkalemia / acidaemia / uraemia
II) Refactory pulmonary oedema
III) toxins / drugs
Treatment of severe hyperkalaemia
Stabilise myocardium:
1. 10ml 10% calcium gluconate
Drive K+ into cells:
2. IV insulin + 25g glucose
3. Salbutamol nebs
Correct acidosis:
4. 1.4% sodium bicarbonate
- Treat cause
Components of nephritic screen - if unexplained AKI/CKD
ANCA (vasculitis)
ANA/ ds DNA (SLE)
Complement (Low in infection/SLE)
Hep B/C screen
Primary causes of Nephrotic syndrome
= immune complex deposition &/or complement activation
Minimal change disease (most common in children)
Focal segmental glomerulonephritis
Membranous glomerulonephritis
Characteristics of nephrotic syndrome
Mean features:
1. Proteinuria
2. Hypoalbuminaemia
3. Oedea - periorbital, legs, scrotal/vaginal
N.B. Periorbital oedema is often noticed first and mistaken for allergy
Others:
- hyperlipidemia
- hypercoagulability
- infections
Consequences of reduced albulin in nephrotic syndrome
Peripheral/periorbital OEDEMA –> Ascites, abdo pain
PLEURAL EFFUSIONS –> SOB, Orthopnoea
Retaining of Na+ and water
Decreased oncotic pressure also a driver for increased lipid synthesis and production of clotting factors
Secondary causes of nephrotic syndrome
= damage due to underlying disease
- Diabetic nephropathy
- SLE
- Infection - hepatitis B/C, HIV, malaria, syphilis
- Drugs (penicillamine, NSAIDs, iron)
- Myeloma
- Pre-eclampsia
- Henoch schonlein purpura (HSP)
What is Minimal change disease?
What is Focal segmental glomerulonephritis?
What is Membranous glomerulonephritis?
What is nephritis?
= inflammation of glomerulus
A specific form of glomerulonephritis
Inflammation –> damage to glomerular capillaries (RBC loss), damage to podocytes (protein loss), reduced GFR
What is glomerulonephritis?
= group of diseases causing immune-mediated inflammation in the glomerulus
A spectrum of Nephrotic and Nephritic syndromes
Nephritis = a specific form of glomerulonephritis
Causes are either:
1. Post-infectious: malaria/staph/salmonella/strep
2: Systemic autoimmune diseases / vasculitis e.g. SLE
Features of nephritis
- Haematuria
- Oliguria (<0.5-1ml /kg/hr)
- Proteinuria
What are red cell casts?
Reflects microscopic bleeding / damage to glomerulus
RBC clump together
Investigations for glomerular disease
- Confirm diagnosis:
- urine dip & MCS
- bloods: U&Es, Cr, Albumin, FBC, ESR, CRP, LFTs
- RENAL BIOPSY - shows microscopic changes to glomerulus - Determine cause:
- autoimmune screen
- Serum & urine immunoglobulins / electrophoresis
- infection screen - Assess complications
- CXR, lipid profile, TFTs, Coag screen
Treatment of nephrotic syndrome
Treatment of Nephritic syndrome
Nephrotic range proteinuria
> 3.5g/d
What condition produced “Cola coloured” urine?
Glomerulonephritis/ Nephritic syndrome
Causes of Raised anion gap metabolic acidosis
- lactic acidosis:
- A: sepsis, shock, hypoxia, burns
- B: metformin - ketones:
- diabetic ketoacidosis
- alcohol - urate: renal failure
- acid poisoning: salicylates, methanol
Causes of normal anion gap metabolic acidosis
- GI bicarbonate loss:
- prolonged diarrhea (may also result in hypokalemia) - Ureterosigmoidostomy fistula
- Renal tubular acidosis
- Drugs: e.g. acetazolamide
- Treatment of metabolic alkalosis (ammonium chloride injection)
- Addison’s disease
Anion gap calculation and normal range
(Na+ + K+) - (Cl- + HCO-3)
Normal = 10-18 mmol/L
CKD stage 1 definition
Greater than 90 ml/min, with some sign of kidney damage on other tests
*if all the kidney tests (proteinurea/U&Es) are normal, there is no CKD
CKD stage 2 definition
60-90 ml/min with some sign of kidney damage
*if all the kidney tests (proteinurea/U&Es) are normal, there is no CKD
CKD stage 3a definition
45-59 ml/min, a moderate reduction in kidney function
CKD stage 3b definition
30-44 ml/min, a moderate reduction in kidney function
CKD stage 4 definition
15-29 ml/min, a severe reduction in kidney function
CKD stage 5 definition
Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
Diuretic used for Ascites
Spironolactone
Features suggesting CKD rather than AKI
Hypocalcaemia (Due to lack of vitamin D)
Characteristics of Diabetes insipidus
high plasma osmolality and a low urine osmolality
Management of nephrogenic diabetes insipidus
thiazides
low salt/protein diet
Treatment of central diabetes insipidus
desmopressin
What is renal tubular acidosis?
Metabolic acidosis due to pathology in the tubules of the kidney
Tubules are responsible for balancing hydrogen and bicarbonate ions and maintaining normal pH
Different types of RTA based upon where along the tubule is affected
Most common types of Renal tubular acidosis
Type 1 - caused by pathology in distal tubule —> unable to excrete hydrogen ions
Type 4 - caused by reduced aldosterone
What is acute tubular necrosis and what causes it?
Necrosis of epithelial cells of the renal tubules
Most common cause of AKI
Damage occurs due to:
- ischaemia (E.g. shock, sepsis, dehydration)
- Toxins (e.g. contrast dye, gentamicin, NSAIDs)
What condition is associated with “muddy brown casts”
Acute tubular necrosis
Relevance of the anion gap?
Reveals whether your blood has an imbalance of electrolytes of if blood is too acidic/alkaline
High +ve = acidosis
Why do patients with CKD develop anaemia?
Reduced erythropoietin levels - most sig. factor
Others
- Reduced erythropoiesis due to toxic effects of uraemia on bone marrow
- Reduced absorption of iron
- Anorexia/nausea due to uraemia
- reduced RBC survival (esp. haemodialysis)
- Blood loss due to capillary fragility and poor platelet function
Treatment of reduced erythropoietin levels due to CKD
Darbepoetin Alfa injections (EPO stimulating)
(Check for other causes of anaemia first)
Extra renal features of autosomal dominant polycystic kidney disease
Hepatic cysts
Diverticulosis
Intracranial aneurysms
Ovarian cysts
How is fluid challenge used to identify cause of oliguria?
Pre-renal uraemia - fluid challenge would cause increase in urine output
Intra renal (e.g. acute tubular necrosis) - poor response to fluid challenge
Urine osmolality in acute tubular necrosis
< 359 mOsm/kg
What are Bence- Jones proteins?
Found in urine in multiple myeloma
They are immunoglobulin light chains found in excessive quantities
