Renal Flashcards
What stones are formed in the presence of increased urinary ammonia and alkaline urine (>7.2)
Struvite
Most common cause of a renal stone
Calcium Oxalate
Hypercalciuria is a major risk factor
Electron microscopy:
The basement membrane is thickened with subepithelial electron dense deposits.
This creates a ‘spike and dome’ appearance
Membranous glomerulonephritis
Management of Membranous glomerulonephritis
ACE inhibitor or an angiotensin II receptor blocker
Causes of anaemia in renal failure
Reduced erythropoietin levels
Reduced absorption of iron
Diabetes insipidus
Either a decreased secretion of antidiuretic hormone from the pituitary (cranial DI)
or
an insensitivity to antidiuretic hormone (nephrogenic DI).
Patients with type one diabetes nearing end stage renal failure should be considered for ?
Joint pancreas and renal transplants.
Membranous glomerulonephritis
Commonest type of glomerulonephritis in adults.
It usually presents with nephrotic syndrome or proteinuria.
Anti-glomerular basement membrane (GBM) disease
Goodpasture’s Syndrome
Small-vessel vasculitis
Pulmonary haemorrhage
Rapidly progressive glomerulonephritis.
Renal Biopsy in Anti GBM disease
Linear IgG deposits along the basement membrane
Management in Anti GBM disease
Plasma exchange (plasmapheresis)
Steroids
Cyclophosphamide
Haemolytic uraemic syndrome
Acute kidney injury
Microangiopathic haemolytic anaemia (MAHA)
Thrombocytopenia
Classically Shiga toxin-producing Escherichia coli (STEC) 0157:H7
Nephrotic syndrome (Triad)
Heavy proteinuria >3 g/day
Low serum albumin <25 g/L
Oedema
Alport’s syndrome
X-linked dominant pattern
Defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM)
Electron microscopy
Longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance
Alport’s Syndrome
Management:
Nephrogenic diabetes insipidus
Thiazides
Low salt/protein diet
Management:
Cranial diabetes insipidus
Desmopressin
Histology:
Mesangial hypercellularity, positive immunofluorescence for IgA & C3
IgA Nephropathy
Berger’s Disease
Fanconi syndrome
Generalised reabsorptive disorder of renal tubular transport in the PCT
Type 2 (proximal) renal tubular acidosis
Polyuria
Aminoaciduria
Glycosuria
Phosphaturia
Osteomalacia
Most common Drug causes of Acute Interstitial Nephritis
Penicillin
Rifampicin
NSAIDs
Allopurinol
Furosemide
Anion gap
(Na+ + K+) - (Cl- + HCO-3)
Metabolic acidosis is commonly classified according to the anion gap
Causes of Normal anion gap
(hyperchloraemic metabolic acidosis)
Gastrointestinal bicarbonate loss:
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison’s disease
Causes of Raised anion gap
Lactate
Ketones:
Urate: renal failure
Acid poisoning: salicylates, methanol
Causes of Unilateral Hydronephrosis
PACT:
Pelvic-ureteric obstruction (congenital or acquired)
Aberrant renal vessels
Calculi
Tumours of renal pelvis
Causes of Bilateral Hydronephrosis
SUPER:
Stenosis of the urethra
Urethral valve
Prostatic enlargement
Extensive bladder tumour
Retro-peritoneal fibrosis
Churg-Strauss syndrome
Late-onset asthma
Vasculitis
Eosinophilia
Nephrotic syndrome: complications
Increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
Hyperlipidaemia - increasing risk of acute coronary syndrome, stroke.
Chronic kidney disease
Increased risk of infection due to urinary immunoglobulin loss
Hypocalcaemia (vitamin D and binding protein lost in urine)
Renal biopsy:
Effacement of foot processes on electron microscopy
Focal segmental glomerulosclerosis (FSGS)
+ Minimal Change disease
Time taken for an arteriovenous fistula to develop
6 to 8 weeks.
Focal or diffuse lupus nephritis - treatment
Glucocorticoids with either mycophenolate or cyclophosphamide is the initial treatment of choice
What is is homologous to TSH in structure and therefore can lead to hyperthyroidism
hCG
Chlorthalidone - MOA
Thiazide Diuretic
IgA nephropathy management
no proteinuria, normal GFR
Observe
IgA nephropathy management
Proteinuria
ACE inhibitor
IgA nephropathy management
Significant fall in GFR/not responding to ACE inhibitor
Corticosteroid
For patients with chronic kidney disease, investigations for anaemia should be considered if ?
Haemoglobin falls below 110g/L
OR
They develop symptoms suggestive of anaemia
Management of Focal segmental glomerulosclerosis
Steroids +/- immunosuppressants
Indications for urgent dialysis
- K > 6.5 even after appropriate medical management
- Symptomatic uraemia
- Pulmonary oedema resistant to full medical management
- Metabolic acidosis pH <7.1
- To remove certain toxins from body e.g. lithium
Absolute contraindications to renal biopsy
Hydronephrosis
Polycystic kidneys
Urinary tract obstruction,
Uncontrolled hypertension
Significant renal malignancy
Significant bleeding disorders.
Hepatitis B infection - what kidney pathology
Membranous glomerulonephritis
Management:
Nephrogenic diabetes insipidus
Thiazides
Low salt/protein diet
Treatment of central diabetes insipidus
Desmopressin
Peritoneal dialysis peritonitis - treatment
Intraperitoneal vancomycin + ceftazidime
Rapidly progressive glomerulonephritis - causes
Goodpasture’s syndrome
Wegener’s granulomatosis
Others: SLE, microscopic polyarteritis
PKD-1 gene - located on chromosome
16
Preferred follow-on agent in lupus nephritis
Mycophenolate
? has been shown to reduce the rate of CKD progression in ADPKD
Tolvaptan
Treatment of Dialysis disequilibrium syndrome
Mannitol or hypertonic saline
? is the treatment of choice for HIV-associated nephropathy
Antiretroviral therapy
? staining is diagnostic of amyloidosis
Congo red
Target BP in CKD:
With diabetes or had urinary ACR >70 mg/mmol
130/80mmHg
Target BP in CKD:
Monitored at home (without DM):
Monitored at clinic (without DM):
135/85mmHg
140/90mmHg
IgA nephropathy management
No proteinuria, normal GFR: ?
Proteinuria: ?
Signifcant fall in GFR/not responding to ACE inhibitor: ?
No proteinuria, normal GFR: observe
Proteinuria: ACE inhibitor
Signifcant fall in GFR/not responding to ACE inhibitor: corticosteroid
