Renal Flashcards
Metabolic Acidosis
Increase in H+ or decrease in HCO3-
Can have a change in anion gap DKA Lactic acidosis Renal failure- increase urate Acid poisoning
Or no change in anion gap
Diarrhoea
RTA
Addisons
Metabolic alkalosis
Decrease H+ or increase HCO3-
Vomiting HypoK+ Diuretics Cushings Primary hyperaldosteronism
Respiratory Alkalosis
Decrease in CO2
Hyperventilation PE Pregnancy Altitude Stroke Subarachnoid haemorrhage
Respiratory Acidosis
COPD
Asthma exacerbation
Sedative drugs- benzodiazepines, opiate overdose
Acute interstitial nephritis
Oedema and interstitial infiltrates of the renal tubules.
Cause of AKI
The causes of AIN:
Drugs (mainly)- Abx (penicillin, rifampicin), NSAIDs, furosemide and allopurinol.
Systemic- SLE, sarcoidosis, Sjorgrens syndrome.
Presentation: Rash, arthralgia, eosinophilia, mild renal impairment, hypertension, fever
Investigate with a white cell cast and sterile pyuria
AKI
Causes
Presentation
Acute damage to the kidneys leading to fluid imbalance (overload/oliguria) and electrolyte imbalance.
Causes:
Pre renal- Ischaemia due to RAS or hypovolaemia
Renal- Autoimmune or toxicity to the glomeruli, tubules or interstitium; GN, rhabdomyolysis, drugs (aminoglycosides, NSAIDs or ACEi/ARBs), RTA, AIN etc
Post renal- Obstruction due to renal stone, external compression of ureter (tumour) or BPH
Presentation: Usually asymptomatic but can present with pulmonary/peripheral oedema, arrhythmias (K+) or oliguria.
RF for AKI
>65yrs Heart failure DM Previous AKI CKD Medication (NSAIDs, aminoglycosides, ACEi/ARBs)
Diagnosis of AKI
Increase in serum creatinine by 26microM in 24hrs
Increase in serum creatinine by >50% in 7 days
<0.5ml/kg/hr urine output for >6hrs
Management of AKI
Supportive
Stop NSAIDs, ACEi/ARBs, aminoglycosides and loop diuretics
Increased toxicity to metformin, lithium and digoxin so stop these.
K+ increase-
IV calcium gluconate for the myocardium
Dextrose+insulin combined to reduce K+
Dialysis/Loop diuretics to remove K+
AKI vs CKD
CKD will see bilateral small kidneys expect in the case of ADPKD, DM or HIV.
HypoCa in CKD
ADPKD
Autosomal dominant PKD
The most common inherited disorder of the kidney, mainly by PKD gene 1 as opposed to PKD 2
Screening for relatives with abdominal USS:
2 cysts in uni/bilateral if <30yrs
2 cysts in both kidneys if 30-59yrs
4 cysts in both kidneys if >60yrs
Treat with tolvaptan if rapidly progressing or CKD 2/3.
Features: HTN, haematuria, recurrent UTIs, CKD, abdominal pain and renal stones.
Extra renal manifestations- Liver cysts mainly, berry aneurysms, can also get cysts at other organs I.e. pancreas
Alport’s syndrome
Inheritited autosomal dominant
Defect in gene for col IV therefore get abnormal GBM.
Young, progressive renal failure, bilateral sensorineural hearing loss, microscopic haematuria.
In transplant pt present with GP syndrome
Diagnose with genetic testing or renal biopsy.
Goodpastures syndrome
Anti GBM against collagen IV leading to pulmonary haemorrhages (increased risk in smoking, young male and LRTI) and rapidly progressing GN.
Treat with plasmapheresis, steroids or cyclophosphamide.
Detect with renal biopsy
CKD Bone disease Anaemia HTN Proteinuria
Bone disease: Usually get hydroxylation of VitD in the kidneys- this not possible therefore get a decrease in Ca and Vit D. Usually get phosphate excretion but can’t therefore get increase PO42-. To sort this out get secondary hyper parathyroidism. Treat with reduced phos in diet, phos binders, Vit D, may need prathyroidectomy. Can cause osteoporosis, osteosclerosis, osteomalacia.
Anaemia: Due to reduced erythropoiesis (get LVH), reduced iron. Always check iron status first. Could also be due to haemodialysis (damage to RBC), toxic uraemia in the BM.
HTN: Most CKD pts will need the meds to treat. Treat with ACEi, expect a decrease in GFR by 25% or increase in serum creatinine by 30%.
Proteinuria: Use ACR. Check in spot sample, from first pass morning urine. ACR>2.5 in diabetics- microalbuminuria
CKD causes
ADPKD DM Chronic GN Chronic pyelonephritis Hypertension
Diabetes insipidus
Polyuria, polydipsia
Central; Can’t produce ADH- idiopathic, head injury, pituitary surgery, haemochromatosis. Treat with desmopressin
Nephrogenic; Insensitive to ADH- genetic, electrolytes (hyperCa or HypoK), lithium pyelonephritis etc. Treat with diuretics (thiazide) and low salt/protein diet.
Water deprivation test
High plasma osmolality but low urine osmolality
Diabetic nephropathy management
Tight glycaemic control Tight BP control Monitor ACR Protein restricted diet Control dyslipidaemia (statins)
FSGS
Common in children Type of nephrotic syndrome Can be inherited (Alports), idiopathic, HIV. Investigate with renal biopsy Manage with steroids/immunosuppressants
NB ensure to treat to avoid remission
Haematuria
Non visible transient; sex, strenuous exercise, menstruation or UTI.
Non visible persistent; cancer (bladder, prostate or renal), BPH, stones, prostatitis, urethritis.
Management:
Need urgent referral if
>45yrs old and has NV haematuria post UTI which has not gone even after UTI successfully treated or NV haematuria without UTI.
Non urgent referral if
Age 60 or over
Also check the U+E, dipstick, BP, ACR
Haemolytic Uraemic Syndrome
Mainly in young children, often caused by shigella toxin E.coli. Also caused by pneumococcal infection, HIV.
Triad: AKI, thrombocytopenia, microangiopathic haemolytic anaemia.
Treat supportively with fluid, blood transfusion and dialysis if required. NB Abx not required.
HypoK
Muscle weakeness, decreased tone, increased predisposition to digoxin toxicity.
Membranous GN
Most common cause of GN.
Thickened GBM with some and spike appearance.
Causes; idiopathic, drugs, malignancy, autoimmune (SLE).
Management includes ACEi/ARBs for everyone, some cases may require immunosuppression.
Prognosis:
1/3 spontaneous remission
1/3 remain proteinuric
1/3 develop ESRF
Minimal change disease
Common form of GN in children.
Causes; idiopathic, drugs (NSAIDs/rifampicin), glandular fever.
Manage with steroids, if unresponsive then with cyclophosphamide.
Prognosis:
1/3 just one episode
1/3 infrequent relapses
1/3 frequent relapses which stop before adulthood.
Nephrotic syndrome
Membranous GN, FSGS, Minimal change disease, diabetic nephropathy.
Complications: Thromboembolism due to increase loss of antithrombin III and plasminogen. (DVT, PE, can occlude renal artery therefore rapid renal failure) Hyperlipidaemia- increase risk of ACS CKD Increased infection HypoCa
Contrast nephrotoxicity
An increase in serum creatinine by more than 25% over 3 days since contrast administration.
Should give IV NaCl 12 hrs pre and post procedure as prophylactic measure.
Peritoneal dialysis
Easier dialysis method for young or those who do not want to go into hospital often.
Side effects include peritonitis (by staph) or sclerosing peritonitis.
Post strep GN
Think if 7-14 days post strep infection, child presenting with malaise, headache, visible haematuria, proteinuria (oedema), HTN.
Bloods will show low complement
Causes of rapidly progressing GN
It is a nephritic syndrome.
Caused by Goodpastures syndrome, Wegeners granulomatosis, SLE
Haematuria with red cell casts
Features of RAS
CKD
HTN
Flash pulmonary oedema
RRT
For when pts are in renal failure, GFR<15.
Haemodialysis: Requires hospital visit. Need to make an arteriovenous fistula 8wks beforehand.
Site infection, air embolism, endocarditis, hypotension.
Peritoneal dialysis: Can continue activities whilst the dialysis occurs the abdomen or have the dialysis occur overnight whilst sleeping.
Peritonitis, sclerosing peritonitis, catheter infection, hernia.
Renal transplant: Average wait being 3 years.
Rejection (need lifelong IS), DVT/PE, infection, BM suppression etc.
Rhabdomyolysis
Usually caused after a fall/ prolonged epileptic seizure- lying down for long period leading to muscle breakdown. Also can be due to drugs I.e. statins.
Leads to AKI, increase CK, myoglobinuria, HypoCa (bound by MG), metabolic acidosis, hyperK.
Spironolactone
Aldosterone receptor antagonist
Used for HF, hypertension, ascites, nephrotic syndrome, conns syndrome
SE: hyperK, gynaecomastia
Sterile pyuria
Partially treated UTI ADPKD Renal stone Urethritis Bladder/renal cell cancer Appendicitis
