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Renal

QuestionAnswer
Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic young adults. Causes idiopathic other renal pathology e.g. IgA nephropathy, reflux nephropathy HIV heroin Alport's syndrome sickle-cell Investigations renal biopsy focal and segmental sclerosis and hyalinosis on light mi
Ultrasound diagnostic criteria (in patients with positive family history) ADPKD two cysts, unilateral or bilateral, if aged < 30 years two cysts in both kidneys if aged 30-59 years four cysts in both kidneys if aged > 60 years
Rapidly progressive glomerulonephritis epithelial crescents in the majority of glomeruli. Causes Goodpasture's syndrome Wegener's granulomatosis SLE, microscopic polyarteritis Features nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria features specific
Normal anion gap ( = hyperchloraemic metabolic acidosis) gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula renal tubular acidosis drugs: e.g. acetazolamide ammonium chloride injection Addison's disease
criteria for diagnosing AKI 1. Rise in creatinine of 26 micromol/L or more in 48 hours OR 2. >= 50% rise in creatinine over 7 days OR 3. Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) OR 4. >= 25% fall in eGFR in children / you
Refer to a nephrologist if any of the following apply: 1. Renal tranplant 2. ITU patient with unknown cause of AKI 3. Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma 4. AKI with no known cause 5. Inadequate response to treatment 6. Complications of AKI 7. Stage 3 AKI (see guideline for
IgA GN associated conditions alcoholic cirrhosis coeliac disease/dermatitis herpetiformis Henoch-Schonlein purpura
markers of poor prognosis in IgA nephritis : male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD
Causes of Polyuria Common (>1 in 10) diuretics, caffeine & alcohol diabetes mellitus lithium heart failure Infrequent (1 in 100) hypercalcaemia hyperthyroidism Rare (1 in 1000) chronic renal failure primary polydipsia hypokalaemia Very rare (<1 in 10 000) diabetes insipi
Nephrotic syndrome: complications Complications increased risk of infection due to urinary immunoglobulin loss increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine. This may result in a renal vein thrombosis, resulting in a sudden deteriorat
CMV in transplanted CMV infection presents with a mononucleosis-like syndrome with fever, myalgia and arthralgia. There is often a leukopaenia, atypical lymphocytosis with a mild rise in transaminases and graft dysfunction. Specific organ involvement can lead to hepatitis,
complications of AV fistula infection thrombosis may be detected by the absence of a bruit stenosis may present with acute limb pain steal syndrome
Causes of cranial DI idiopathic post head injury pituitary surgery craniopharyngiomas histiocytosis X DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome) haemochromatosis
Rhabdomyolysis causes seizure collapse/coma (e.g. elderly patients collapses at home, found 8 hours later) ecstasy crush injury McArdle's syndrome drugs: statins (especially if co-prescribed with clarithromycin) overexertion, compartment syndrome, drugs eg. statins, neurolepti
Rhabdomyolysis features acute kidney injury with disproportionately raised creatinine elevated creatine kinase (CK) myoglobinuria hypocalcaemia (myoglobin binds calcium) elevated phosphate (released from myocytes) hyperkalaemia (may develop before renal failure) metabolic acido
Causes of nephrogenic DI genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel electrolytes: hypercalcaemia, hypokalaemia drugs: demeclocycline, lithium tubulo-intersti
Dialysis disequilibrium syndrome results in cerebral oedema which can present as focal neurological deficits, papilloedema and a decreased level of consciousness. It can be treated with mannitol or hypertonic saline likely to occur in patients with very high levels of urea, metabolic a
Amyloidosis: types AL amyloidosis the most common form of amyloidosis L for immunoglobulin Light chain fragment due to myeloma, Waldenstrom's, MGUS features include: nephrotic syndrome, cardiac and neurological involvement, macroglossia, periorbital eccymoses AA amyloid
ADPKD: features Features hypertension recurrent UTIs abdominal pain renal stones haematuria chronic kidney disease Extra-renal manifestations liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly berry aneurysms (8%): rupture can cause su
Testicukar Ca The peak incidence for teratomas is 25 years and seminomas is 35 years. Risk factors include: infertility (increases risk by a factor of 3) cryptorchidism family history Klinefelter's syndrome mumps orchitis
Acute interstitial nephritis causes drugs: the most common cause, particularly antibiotics penicillin rifampicin NSAIDs allopurinol furosemide systemic disease: SLE, sarcoidosis, and Sjögren's syndrome infection: Hanta virus , staphylococci
Factors which increase the likelihood of pulmonary haemorrhage in Goodpasture smoking lower respiratory tract infection pulmonary oedema inhalation of hydrocarbons young males
Acute interstitial nephritis Causee drugs: cephalosporin, penicillin, clarithromycin, rifampicin, NSAIDs, allopurinol, furosemide systemic disease: SLE, sarcoidosis, and Sjögren's syndrome infection: Hanta virus , staphylococci, legionella, CMV, streptococcal)
Features Acute interstitial nephritis fever, rash, arthralgia eosinophilia in the urinalysis mild renal impairment hypertension
Treatment of Goodpasture's has three main principles: Remove any identifiable cause of antibody production. Exposure to organic solvents, hydrocarbons, metal dust and smoking are known to increase the risk of developing the disease. Stop further antibody production using immunosuppressive medication (cyclop
Plasmapheresis in Goodpasture's is indicated in the following: . anti-GBM disease in patients with pulmonary haemorrhage those with renal involvement who do not require renal replacement therapy at presentation (the indication in this case) selected patients who may require dialysis but present acutely, are young an
Rapidly progressive glomerulonephritis Causes Goodpasture's syndrome Wegener's granulomatosis others: SLE, microscopic polyarteritis
ECG features hypokalamia U waves small or absent T waves prolonged PR interval ST depression
Risk factors of Nephrotoxicity due to contrast media known renal impairment (especially diabetic nephropathy) age > 70 years dehydration cardiac failure the use of nephrotoxic drugs such as NSAIDs
Prevention of nephrotoxicity due to contrast media the evidence base currently supports the use of intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure. There is also evidence to support the use of isotonic sodium bicarbonate
Features of ADPKD ADPKD: features hypertension recurrent UTIs abdominal pain renal stones haematuria chronic kidney disease
Extra-renal manifestations of ADPKD liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly berry aneurysms (8%): rupture can cause subarachnoid haemorrhage cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic
Prevention of renal stones Calcium stones may be due to hypercalciuria, which is found in up to 5-10% of the general population. high fluid intake low animal protein, low salt diet (a low calcium diet has not been shown to be superior to a normocalcaemic diet) thiazides diuretic
what increases the risk of AKI: 1. Emergency surgery, ie, risk of sepsis or hypovolaemia 2. Intraperitoneal surgery 3. CKD, ie if eGFR < 60 4. Diabetes 5. Heart failure 6. Age >65 years 7. Liver disease 8. Use of nephrotoxic drugs
It also defines the criteria for diagnosing AKI 1. Rise in creatinine of 26 micromol/L or more in 48 hours OR 2. >= 50% rise in creatinine over 7 days OR 3. Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) OR 4. >= 25% fall in eGFR in children / you
Refer to a nephrologist if any of the following apply: 1. Renal tranplant 2. ITU patient with unknown cause of AKI 3. Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma 4. AKI with no known cause 5. Inadequate response to treatment 6. Complications of AKI 7. Stage 3 AKI (see guideline for
Haemolytic uraemic syndrome is generally seen in young children and produces a triad of: acute kidney injury microangiopathic haemolytic anaemia thrombocytopenia
causes of secondary (termed 'typical HUS'): classically Shiga toxin-producing Escherichia coli (STEC) 0157:H7 pneumococcal infection HIV rare: systemic lupus erythematosus, drugs, cancer
sevelamer a non-calcium based binder that is now increasingly used binds to dietary phosphate and prevents its absorption also appears to have other beneficial effects including reducing uric acid levels and improving the lipid profiles of patients with chronic ki
Features of renal cell carcinoma classical triad: haematuria, loin pain, abdominal mass pyrexia of unknown origin left varicocele (due to occlusion of left testicular vein) endocrine effects: may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH
Causes of Fanconi syndrome cystinosis (most common cause in children) Sjogren's syndrome multiple myeloma nephrotic syndrome Wilson's disease
HIV-associated nephropathy (HIVAN) accounts for up to 10% of end-stage renal failure cases in the United State. features of HIVAN: massive proteinuria resulting in nephrotic syndrome normal or large kidneys focal segmental glomerulosclerosis with focal or global capillary collapse on rena
Created by: Dr.Selma