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CBL nephro
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- 1Where does oedema first present in children?periorbital
- 2What might frothy urine indicate?proteinuria
- 3common cause of nephrotic syndrome in childrenminimal change nephropathy
- 4initial investigation in nephrotic syndromeFBC
Serum biochemistry – renal function, liver function, bone profile
Urine biochemistry - protein:creatinine ratio (PCR)
Serum bacteriology - Anti-Streptolysin O (ASO) titre
Serum immunology - complement (C3, C4)
Note that renal ultrasound is less commonly performed in children than in adults, in whom the range of likely diagnoses is broader - 5Which children may benefit from renal biopsy in diagnosis?children aged <1 or >12 are likely to undergo renal biopsy as minimal change nephropathy, while still the likely diagnosis, is not such a dominant possibility.
- 6Management of minimal change nephropathy when biopsy?Oral corticosteroid (prednisolone) until urinalysis negative for protein, then taper down
Biopsy if findings or progress atypical eg if poor response to 1 month of steroid, suggesting that the diagnosis is not, after all, minimal change nephropathy - 7investigations in adult with nephrotic syndrome- FBC, coagulation screen
- Serum biochemistry – renal function, liver function, bone profile, lipids, glucose
- Urine biochemistry - PCR, BJP
- Serum immunology – ANA, ANCA, complement, Igs, free light chains
- Renal ultrasound
- CXR
- Renal biopsy
- ECG - 8immunology tests in secondary nephrotic syndrome
- 9Membranous nephropathy histologythickened capillary loops, normal cellularity
- 10—On light microscopy a silver stain highlights in black the proteinaceous material in the thickened basement membranes. There are characteristic “spikes” of basement membrane between the immune deposits seen on electron microscopy
- 11electron microscopy of membranous nephropathy associated with tumoursthe immune deposits are more likely to be heterogeneous in size and shape.
This finding may encourage a low threshold for investigation of symptoms which might indicate occult underlying tumour. - 12immunofluorescence microscopy of membranous nephropathygranular deposits of Ig (immune complex) and complement
- 13Management of membranous nephropathy- Diuretic
- ACE-inhibitor +/or ARB – reduces proteinuria
- Consider anticoagulation and lipid-lowering medication (because of the hypercoagulable state and hyperlipidaemia associated with nephrotic syndrome)
Consider immunosuppressive therapy if renal function deteriorates
If the nephropathy is thought to be secondary eg to tumour, treatment of the underlying cause may lead to remission of the nephrotic syndrome - 14urine in acute glomerulonephritisblood and protein
- 15initial investigations in acute glomerulonephritis- FBC, coagulation
- Serum biochemistry – renal function, -CRP, liver function, bone profile
- Urine biochemistry – PCR
- Serum bacteriology - Anti-Streptolysin O titre
- Serum immunology – autoantibodies (ANA, ANCA), complement (C3, C4), Igs
- Throat swab – for culture and sensitivity
- Renal ultrasound
Renal biopsy if renal function worsens, or if proteinuria and haematuria fail to resolve once throat does, or if autoantibody testing proves positive - 16investigation results in IgA nephropathyhigh serum IgA
high PCR
? Strep - 17management of IgA nephropathySymptomatic
May give antibiotic to clear streptococcus if present
Further treatment if indicated by biopsy if performed - 18histopathology of IgA nephropathyProliferation of mesangial cell matrix and hypercellularity with IgA deposits in mesangium on immunofluorescence.
- 19IgA nephropathy clinical presentationspectrum of pathological findings with variable clinical manifestations. Can also present with Henoch-Schoenlein prupura.
- asymptomatic urinary abnormalities
- visible haematuria
- accute GN with rapidly declining kidney function
- chronic decline in kidney function with hypertension - 20significance of red cell castsalways pathological, and is strongly indicative of granulomatosis with polyangiitis, systemic lupus erythematosus, post-streptococcal glomerulonephritis or Goodpasture's syndrome
--> crescentic nephropathy - 21—Active crescent obliterating Bowman’s space and compressing glomerular tuft
- 22Management of Wegener's granulomatosisCorticosteroid, cyclophosphamide and plasma exchange
may require haemodialysis - 23Wegener's symptoms
- 24risk factors for rhabdomyolysis- seizures
- drugs
- local heat
- lying
- alcohol
- opiates - 25Appearance of myoglobinuriachocolate brown urine
false positive dipstick haematuria result - 26What is the significance in renal units of blood borne viruses?with ample evidence of transmission within Renal Units, we are keen to immunise long-term dialysis patients against hepatitis B.
We also isolate patients and/or their haemodialysis machines if patients test positive for blood-borne viruses or do not consent to be tested - 27How is rhabdomyolysis diagnosed?- raised CK
- myoglobin in blood and urine
- raised K+
- raised creatinine - 28How does rhabdomyolysis cause acute kidney damage?1–2 days after the initial muscle damage
due to accumulation of myoglboin in the renal tubules - 29Why bone profile in rhabdomyolysis?lots of phosphate in muscle
when released stimulates PTH production, causing resorption of calcium from bone - 30effect of hypocalcaemiafits --> arrhythmia
- 31emergency treatment of hyperkalaemiacalcium gluconate, dextrose: insulin, dialysis resonium (v slow, make you sick)
Rehydration - 32Why anaemia in CKD?loss of Epo
- 33hyperkalaemia ECGtall, peaked T waves
- 34Why caution with diabetic drugs in CKD?anti-diabetic drugs and insulin have longer half life --> hypoglycaemia
- 35common drug that causes rhabdomyolysisstatins
- 36rare kidney effect of omeprazoleinterstitial nephritis
- 37inital investigations in AKI with multiple contributory factorsFBC
Serum biochemistry – renal function, CRP, liver function, bone profile
Serum gentamicin level
CXR
Renal ultrasound - 38management of AKI with pulmonary oedema- Resuscitation, including correction of hypotension- inotropes difficult with tachyarrhythmia
- Correction of hyperkalaemia
- Treatment of pulmonary oedema with diuretic – or dialysis.
- Withdrawal of potentially nephrotoxic drugs - 39initial investigations in possible advanced CKD- FBC
- serum biochemistry: U&Es, LFTs, bone profile inc. PTH
- renal US
Reticulocyte count, serum B12, folate and ferritin
CXR - 40CKD kidneys on USsmall with reduced cortical thickness
lack of cortico-medullary difference - 41management of CKD first presentationCorrection of metabolic abnormalities associated with renal failure (acidosis, anaemia, hyperparathyroidism
Prepare for dialysis and transplantation - 42post-transplant immunosuppresiontacrolimus
cyclosporin
MMF - 43initial investigations in post-renal transplant diarrhoea caseFBC
Serum biochemistry –renal function, bone profile, liver function, including lactate dehydrogenase (LDH), CRP
CXR - 44management of post-renal transplant opportunistic CMV infection• Minimise immunosuppression
• Specific anti-viral therapy (ganciclovir or valganciclovir)
• If renal function doesn’t normalise consider transplant biopsy - 45What to check in oedema before giving diuretics?albumin
- 46When may occult renal or cardiac disease present?in pregnancy
- 47initial effect of hydronephrosisaffects medulla first, so cannot concentrate urine!
- 48RBC lifespan in CKD80 days
- 49Which drug can cause post-transplant diabetes?Tacrolimus
- 50LDH raised in whatmonitoring injury heart, liver, lung, hematological disorders (lymphoma)
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- Nephrology Fichas sobre CBL nephro, creado por Ellie Britt el 15/01/2018.
- Creado por
- Ellie Britt
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