Renal And GUS Flashcards
criteria for nephrotic syndrome
proteinuria >3.5g in 24h hypoalbuminemia <3g/DL generalised oedema hyperlipidemia and lipiduria (hypercoagubility)
criteria of nephritic syndrome
haematuria
hypertension
proteinuria (less than nephrotic)
oliguria and azotemia
size of largest molecules to be filtered in health
4nm (max diameter of gaps in podocytes) also +> - charge due to negative collagen
mechanism of linear v granular immune deposits in glomeruli
linear: anti-GBM (TIV collagen alpha3 chain)
granular: circulating Ag (endogenous or exogenous) deposited OR Ab v GBM (to PLA2-R in membranous nephropathy only)
exogenous antigens that can deposit in glomeruli
hep C At, HBsAg l, strep protein, treponema, plasmodium.
where are subendothelial deposits in the glomeruli
side near blood
where are subepithelial deposits in glomeruli
on the side near bowman’s capsule.
Risk factors for Renal cell carcinoma?
Smoking, HTN, obesity
Acquired polycystic kidney disease (dialysis) RRx30
Occupational: cadmium, asbestos, pertrol
Chronic analgesia use (paracetamol, aspirin)
Family history
Age and sex for Renal cell carcinoma?
M>F. 60-80y
Classical triad of RCC?
Haematuria
Abdominal pain
Flank mass
(Only present in 10%)
Typical blood findings for RCC?
Anaemia (normocytic) + Raised ALP
Or Hypercalcaemia or polycythaemia
Ways of RCC presentation?
Incidental finding
Classical triad: haematuria, abdo pain, flank mass
Local invasion: IVCO, Buddchiari, scrotal varicocoele, limb oedema
Paraneoplastic: anaemia, B symptoms, cahexia, lytic bone lesions, polycythaemia (EPO), feminisation, masculinisation, HTN, PMR, amyloidosis
Metastatic: (30% at present) lung, lymph, liver, bone, brain,
How would you investigate ?RCC
Urine dip: haematuria (not great) FBC: paraneoplastic syndrome LDH: marker of advanced disease LFTs + coag: metastases, Stauffer's syndrome Corr Ca: raised (advanced disease) U+Es Imaging: US abdo/pelvis OR CT
What is stauffer’s syndrome?
Non-metastatic (paraneoplastic) nephrogenic hepatic dysfunction. Cholestasis (elevated bilirubin, alk phos, GGT) + elevated PT, thrombocytosis and hepatosplenomegaly
DDX for renal mass:
Benign: simple renal cysts (NB. USS to confirm not complex/malignant); or
Angiomyolipoma; or Oncocytoma.
Malignant: renal cell carcinoma, metastases.
How to distinguish oncocytoma from RCC?
With difficulty! But management is similar anyway!
Mx: nephrectomy (to prevent complications/spont haemorrhage)
Biopsy: central stellate scar. Granular cytoplasm (looks like clear cell)
Subtypes of RCC?
Clear cell (65%)
Papillary renal cell (10-15%)
Chromophobe renal carcinomas (5%)
Biochemistry of excess aldosterone?
Hypokalaemic, alkalosis, high to normal sodium.
How to differentiate primary and secondary hyperaldosteronism?
Primary: normal-high Na, HTN, pH high. [renin] plasma LOW
Secondary: low Na (<138), ±HTN, pH maybe normal. (Look for causes: CCF, ascites, nephrotic syndrome) [renin] plasma HIGH
BOTH: K excretion >30mmol pd.
What is Conn’s syndrome?
Primary adrenal disease with excess aldosterone.
signs and symptoms of Conn’s syndrome?
Hypertension, muscle weakness, latent tenant, paraesthesia, polydipsia, polyuria, nocturia
Cause of HTN + low K
Thiazide diuretics
?conn’s syndrome
How to investigate ?raised aldosterone?
[aldosterone]/[renin]
Renin activity + renin mass
If both are low (<800, <80) excludes diagnosis
If both are high (>2000, >200) likely diagnosis
How to confirm diagnosis of Conn’s syndrome?
- Saline suppression test: 2l IVI 0.9% over 4h. Should decrease aldosterone. Diagnostic if aldosterone >140pmol/. (But risk of inducing cardiac failure esp in elderly)
- Sodium loading + fludrocortisone over 4d
But needs admission to hospital and risks of serious hypokalaemia
Causes of conn’s syndrome?
Adrenal adenoma
Bilateral adrenal hyperplasia
GC remediable hyperaldosteronism (genetic)
How to calculate plasma osmolality?
2x[Na] + [urea] + [glucose] (mmol/l)
Diagnostic criteria of SIAD
Hyponatraemia (<135)
Hypo-osmolar plasma <270
Inappropriate concentrated urine >100mmol/kg
No adrenal, renal ro thyroid dysfunction
(Do NOT measure ADH, it’s raised in most people with hyponatraemia anyway)
Causes of hyponatraemia?
(Sick cell, pseudo)
Na losses (hypovolaemic)
Inability to excrete free water (hypervolaemic)
SIAD (normovolaemic)
Management of dilutional hyponatraemia?
(Correct at rate of onset, monitor carefully)
Water restrict
Demclocycline (v ADH-R antag @ collecting duct)
Risk of rapid correction of hyponatraemia?
Central pontine myelinolysis
Urgent correction of dilutional hyponatraemia?
Hypertonic saline (1.8/2.7/3%) to increase [Na] by 1mmol/l/h
(Correct 0.5mmol/l/h if >48h onset)
NOT if fluid overloaded.
Max increase of [Na]plasma per day?
Do NOT correct more than 10mmol/l over 24h.
When to stop treating urgent hyponatraemia?
When Na 120mmol/l or pt asymptomatic
How to correct dilutional hyponatraemia in fluid overloaded pt?
Loop diuretic + hypertonic saline?
Min Na, K, Cl intake pd?
1mmol/kg per day
Min water intake pd?
25-30ml/kg/day
Min glucose needed pd?
50-100g per day
Max K replacement?
<240mmol in 24h
What is Addison’s disease?
Primary adrenal insufficiency. reduced aldosterone and cortisol.
How to distinguish hypervolaemic hyponatraemia due to CKD or CCF?
Urine osmolality: if >20mmol/l suggests renal cause.
Urine osmolality <20mmol/l suggests non-renal cause
Disorders associated with hypokalaemic alkalosis
Liddle’s syndrome
Gitelman’s syndrome
Bartter’s syndrome
Baby presents with polyuria and low BP. Urinary Ca high. Na 138; K 2.8; Urea 3.4; Cr 62; pH 7.51; HCO3 33. Likely diagnosis?
Hypokalaemic Metabolic alkalosis.
Bartter’s syndrome: salt wasting (hypercalciuria, Mg). Impaired Na resorption in LoH (NKCC2 defect)
What is Bartter’s syndrome?
Defect in thick asc LoH. Direct/indirect impairment of NKCC2. Hypokalaemia, alkalosis, hypotension.
Onset 24-30w. High renin and Aldosterone.
Salt wasting: lose Ca, Mg, Cl, K in urine.
PC: polyhydramnios, polyuria, polydipsia
Autosomal recessive
What is Liddle’s syndrome?
Activating mutation in ENaC (DCT Na channel): always active.
Pseudohyperaldosteronism. Retain Na and H2O
PC: infant-early adult. Autosomal dominant.
HTN, hypernatraemia, hypokalaemia (high HCO3, low renin and aldosterone)
4 ways NSAIDs kill the kidneys
Dysregulation of blood flow
Toxic Tubulointerstitial insult
Membranous GN
Minimal change GN
Cause of patchy tubular necrosis?
Renal hypoperfusion/prerenal AKI.
Causes of confluous tubular necrosis?
Exogenous: solvents, gentamycin, heavy metals, radiocontrast
Endogenous: HbC, myoglobin, light chain (myeloma)
Stages of AKI?
1: 1.5xincrease in [Cr] (>0.3mg/dl) OR <0.5ml/kg/h for 6h
2. 2-3xincrease in [Cr] OR <0.5ml/kg/h for >12h
3. >3xincrease in [Cr] OR <0.5ml/kg/h for >24h OR anuria for 12h OR renal replacement therapy needed
Indications for dialysis?
AEIOU Acidosis Electrolytes (K) Ingested toxins Overload Uraemic
Stages of CKD?
(GFR in ml/min)
1: >90 + something else e.g. ACR>3
2. 60-90
3. 30-59
4. 15-49
5. <15 AKA ESRF
