What is nephritic syndrome
Hypertension Blood- Haematuria occurs due to podocytes developing large pores which allows blood and protein to escape into the urine. Some protein Fast onset Low urine volume due to poor function
What is nephrotic syndrome
Proteinuria >3.5g in 24hrs
Oedema
Hypoalbuminaemia
Hyperlipidaemia (by product of increased albumin production)
Causes of nephritic syndrome
Post strep glomerulo nephitis
IgA Nephropathy
DM/ Vasculitis
Rapidly progressive glomerular nephritis
- Goodpastures
- Vasculitis - Wegner’s/ Churg strauss/ microscopic polyangitis
Causes of nephrotic syndrome
Primary:
Minimal change
FSGS
Membranous glomerulonephitis
Secondary:
SLE
Hep B and C
HIV
Diabetes mellitus
Malignancy
Amyloidosis
What is haemolytic uraemic syndrome
Triad of
Thrombocytopenia
Haemolytic Anaemia
AKI
Children
Emergency
Often after food poisoning/ gastroenteritis e.g. E coli, Shigella, Campylobacter
What is minimal change glomerulonephritis
Nephrotic
• Childhood/ adolescence (commonest cause in children)
• Responds to steroids
• May recur
• Usually no progression to renal failure
• Loss of podocytes due to unknown circulating factor (not immune complex)
What is FSGS
• Commonest in adults?
Other end of spectrum from minimal change
• Less responsive to steroids (need ciclosporin etc)
• Fibrosis/ scarring/ glomerulosclerosis
• Circulating factor causes – transplants often it recurs
• Progressive to renal failure
High recurrence in transplants
What is Membranous glomerulonephritis?
- Causes kidney failure in a third of patients
- Immune complex deposits
- Autoimmune (likely) or secondary e.g. lymphoma, lupus or malaria.
- IgG
What happens to kidneys in DM in context of nephrotic?
- Thickening of the basement membrane/ collagen
- Microvascular damage
- Mesangialsclerosis
- Progressive renal failure
Describe IgA nephropathy
- Commonest GN
- Any age
- Haematuria can be invisible
- Mucosal infections relationship
- Variable histology and course
- Possible proteinuria
- Often renal failure
- Mesangial damage and scarring
- Immune complex deposition
- appears within a day or two after a URTI
Describe hereditary nephropathies
• Thin GBM nephropathy • Benign familial nephropathy • Isolated haematuria (blood is normal) • Alport: X linked Abormal collagen IV Associated with deafness Abnormal GBM Progressive to renal failure
What is Goodpastures?
• Uncommon
• Rapidly progressive
• Acute onset of severe nephritic syndrome
• Association with pulmonary haemorrhage (smokers)
• Autoantibody to collagen IV in BM
• Treatable by immune suppression and plasmaphoresis if caught early
(steroids and cyclophosphamide)
• IgG deposition with no Em deposit and inflam cells
Anti GBM
Renin and aldosterone levels in Cushings Conns and Renal artery stenosis. Results?
Cushing’s and Conn’s would be associated with a high aldosterone and a low renin, renal artery stenosis would be associated with a high renin and aldosterone, Liddle’s (genetic) is associated with a low renin and aldosterone.
Hypertension and hypokalaemia
Treatment hyperglycaemia
Manage precipitating factors, stop drugs e,g, ACEi
Stabilisation of the cardiac membrane
intravenous calcium gluconate by slow IV injection titrated to ECG response
Short-term shift in potassium from extracellular to intracellular fluid compartment
combined insulin/dextrose infusion
nebulised salbutamol
Consider NaHCo3 if acidotic
Removal of potassium from the body
calcium resonium (orally or enema)
loop diuretics
dialysis
Cause and treatment of most common solid organ transplant recipiants
Cytomegalovirus
Ganciclovir
Post-op complications of renal transplant
Post-op problems ATN of graft vascular thrombosis urine leakage UTI
Hyperacute acute rejection (minutes to hours)
due to pre-existent antibodies against donor HLA type 1 antigens (a type II hypersensitivity reaction)
rarely seen due to HLA matching
Acute graft failure (< 6 months)
usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
other causes include cytomegalovirus infection
may be reversible with steroids and immunosuppressants
Causes of chronic graft failure (> 6 months)
both antibody and cell mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)
Long term cancer - 25% have cancer after 20 years (often skin)
ABG in sepsis
Patients who have sepsis often have a raised serum lactate due to the hypoperfusion of their peripheries. This gives them a metabolic acidosis with a raised anion gap.
Raised anion gap vs normal?
If the anion gap is raised, this suggests that there is increased production, or reduced excretion, of fixed/ organic acids e.g.
Lactic acid (sepsis, tissue ischaemia)
Urate (renal failure)
Ketones (diabetic ketoacidosis)
Drugs/ toxins (salicylates, methanol, ethylene glycol)
If there is a metabolic acidosis with a normal anion gap, then this is either due to loss of bicarbonate, or accumulation of H+ ions. Causes include: Renal tubular acidosis Diarrhoea Addison's disease Pancreatic fistula
Management of acute renal colic
IM or oral Diclofenac
Alpha-adrenergic blockers to aid ureteric stone passage
US - 45% sensitivity
Non-contast CT if not
Lithotripsy or nephrolithotomy for severe cases. most pass within 4 weeks
<0.5cm then conservative
If assocaited infection then urgent need for decompression so percutaneous nephrostomy (in loin)
If large proximal stone (e.g. 2.3cm staghorn calculi) then pecutaneous nephrolithotomy as lipotrypsy has low clearence rate
Complex stone disease of CI of lithotripsy (preggers) then ureteroscopy
Prevention of 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 diuretics (increase distal tubular calcium resorption)
Oxalate stones
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion
Uric acid stones
allopurinol
urinary alkalinization e.g. oral bicarbonate
factors which effect eGFR
pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being take
eGRF variables
CAGE - Creatinine, Age, Gender, Ethnicity
Complications in peritoneal dialysis
peritonitis: coagulase-negative staphylococci such as Staphylococcus epidermidis is the most common cause. Staphylococcus aureus is another common cause
sclerosing peritonitis
Way of diagnosing ATN
ATN rest the kidney, no fluid - one litre restriction. If you get brown cell card, fraction of Na in urine - More than 1% in urine = ATN.
Damage to tubular cells due to prolonged ischaemia or toxins
Kidneys can no longer concentrate urine or retain sodium - urine osmolality low, urine sodium high
Staging of AKI
Stage Creatinine Urine production
1 Increase 1.5-1.9x baseline < 0.5ml/kg/h for >6 consecutive hours
2 Increase 2.0-2.9x baseline < 0.5ml/kg/h for >12 consecutive hours
3 Increase > 3x baseline or >354 µmol/L < 0.3ml/kg/h for > 24h or anuric for 12h
3 also is renal replacement therapy
Only one thing needed
Causes of transient or spurious non-visible haematuria
urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse
Causes of persistent non-visible haematuria
cancer (bladder, renal, prostate) stones benign prostatic hyperplasia prostatitis urethritis e.g. Chlamydia renal causes: IgA nephropathy, thin basement membrane disease
Testing of haematuria
urine dipstick is the test of choice for detecting haematuria
persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart
renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked
urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected
When to refer for haematuria for cancer screening
Urgent
>45 and unexplain visible haematuria (no UTI
Non-urgent
Aged >60 with recurrent or persistent unexplained UTI
What is Henoch- Schonlein purpura
palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure
analgesia for arthralgia
treatment of nephropathy is generally supportive. There is inconsistent evidence for the use of steroids and immunosuppressants
Self limiting
Causes of hypokalaemia
1.) Increased potassium loss:
Drugs: thiazides, loop diuretics, laxatives, glucocorticoids, antibiotics
GI losses: diarrhoea, vomiting, ileostomy
Renal causes: dialysis
Endocrine disorders: hyperaldosteronism, Cushing’s syndrome (OBVIOUSLY spirono is aldosterone antagonist)
2.) Trans-cellular shift Insulin/glucose therapy Salbutamol Theophylline Metabolic alkalosis
- ) Decreased potassium intake
- ) Magnesium depletion (associated with increased potassium loss)
Treatment hypokalaemia
Mild to mod 2.5-3.4 = oral KI if asymptomatic and no ECG changed
Severe hypokalaemia <2.5 or symptomatic = IV replacement, ITU/ cardiac monitoring. If no CI to fluiod therapy e.g. HF, then dilute to low concs to avoid plebitis. Don’t exceed 20mmol/hr
What is ADPKD
Aut dom polycystic kidney disease
1/1000 Caucasians
Two loci PKD1 and 2 polycystin-1 and 2
Type 1 presents earlier
US diagnosed based on age and number of cysts 2 or more and <60. 4 in both aged >60
Enlarged kidney
How to tell DI?
Water suppression test -
Stage 1 - no drink for 8 hours, measure weight and urine osmolality
Stage 2 - Give Desmopressin (like ADH) if nephrogenic there will be no response
Treatment of DI
Nephrogenic = Chlorothiazide Cranial = desmopressin (synthetic vasopressin)
Features of chlamydia
asymptomatic in around 70% of women and 50% of men
women: cervicitis (discharge, bleeding), dysuria
men: urethral discharge, dysuria
Symptoms of anaemia in CKD
Tachy
Pale
Aoritc flow murmur
Predispsosition to LVH
Causes of anaemia in renal failure
reduced erythropoietin levels - the most significant factor
reduced erythropoiesis due to toxic effects of uraemia on bone marrow
reduced absorption of iron
anorexia/nausea due to uraemia
reduced red cell survival (especially in haemodialysis)
blood loss due to capillary fragility and poor platelet function
stress ulceration leading to chronic blood loss
How to calculate anion gap?
([Na+] + [K+]) - ([Cl] + [HCO3]) (how many anions extra)
The anion gap is used to classify metabolic acidosis into either;
Raised anion gap seen in e.g. diabetic ketoacidosis or,
Normal anion gap seen in patients with diarrhoea due to gastrointestinal bicarbonate loss.
Side effects of EPO
accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients)
bone aches
flu-like symptoms
skin rashes, urticaria
pure red cell aplasia* (due to antibodies against erythropoietin)
raised PCV increases risk of thrombosis (e.g. Fistula)
iron deficiency 2nd to increased erythropoiesis
Diabetes inspidius is characterised by what biochem?
Diabetes insipidus is characterised by a high plasma osmolality and a low urine osmolality
Signs of hypovolaemia
Low BP, tachy, poor tissue turgor (hand pinch), sunken eyes, dry mucous membranes, daily weight loss, low urine output, cap refil.
Cap refil, BP, skin turgor are late chanes
Signs of hypervolaemia
High BP, High JVP, weight gain, high urine output, lung crepitaions, periopheral oedema, gallop rhythm
When to use colloid?
Blood for haemorrhage. HAS in speciallist use for hepatorenal syndrome
Controversy regarding HCO3 in acidosis
Generate CO2 - adequate ventilation needed to prevent resp acidosis worsening
NaHCO3 given so NA load and volume load which can cause fluid overload.
Treat cause and in AKI may need RRT
Possible indications for RRT in AKI
INdividual but suggestions:
Persistent acidosis or hyperkalaemia
Uraemia
Fluid overload unresponsive
Complications of RRT
Bleeding from anti coag Damage from catheter Drug accumulation/ clearence Altered nutrition Procedural hypotension
Symptoms/ complications of AKI
Hyperkalaemia Hypertension Uraemia Pericarditis Acidosis Confusion Coma Fluid overload
Pre renal causes AKI
Hypotension/ dehydration Vascular volume decrease e.g. haemorrhage CO decrease e.g. cardiogenicshocl, MI Peripheral vasodilation e.g. sepsis, drugs Renal artery stenosis Renal vasoconstriction NSAIDS, ACEi HRS
Renal causes AKI
INterstitial
Gentamicin, Cephalosporin, Lithium, Diuretics, pyelonephritis, infiltration e.g. sarcoid
Glomerular disease e.g. FSGS Goodpastures, Glomerulonephritis, ATN (prolonged hypoperfusion)
Vessels e.g. Vasculitis, Haemolytic uraemic syndrome, Thrombotic thrombocytopenic papura (autosomal recessive), DIC (due to cancers, trauma, sepsis, infection, allergy, aortic aneurisms)
Post renal causes AKI
Ureteric stricture Renal calculi Transition cell Carcinoma Pelvic mass Iatrogenic ureter damage
RFs AKI
CKD CVD Maligancy Age Male CliverD Complex surgery
Initial management of AKI
NEWS >7 consider ITUK+ ECG - potassium Treat if >6.5 or ECG change Examine BP - fluid trial 500ml in 15min x 4
Monitoring of AKI
Catheter
K+Obs every 4 hrs
Lactate if signs of sepsis
Daily creatine (24hr behind response)
Investigations AKI
Urine dip
USS kidney LFTs (HRH) Thombocytopenia (if yes then bloodfilm for HUS) Intrinsic renal disease Igs Complement ANA ANCE Anti-GBM
Supportative treatment AKI
Sepsis
Stop nephrotoxic meds
Stop drugs that may cause comps e.g. diuretics (K) metformin (acidosis), antihypertensives
Check drug doses
Gastroprotection and nutritional support
Avoid contrast
Consider referral e.g. stage 3
More defiinitve treatment AKI
Refer to renal team if comps or stage 3 AKI Depends on cause Renal - biopsy and refer Post renal Catheter Nephrostomy Urological interventio Mange fluid balance, acidosis, hyperkalaemia
Complications of nephrotic syndrome
Loss of AT3, C and S - rise in fibrogen predispose to thrombosis
Los of Thyroxine binding globulin but not free thyroxine
Signs and nsymptoms of polycystic kidney disease
HTY - RAAS overactivity Headache Haematuria Polyuria Back pain Cyst infections
Treatment polycystic
Dietary restrictions
RRT
What is diffuse proliferative glomerulonephritis?
classical post-streptococcal glomerulonephritis in child
presents as nephritic syndrome / acute kidney injury
most common form of renal disease in SLE
What is clot retention??
Clot retention occurs as a sequal to bleeding in the urological tract. Large clots can become wedged in the urethra and cause acute urinary retention.
It can be seen under any circumstance where there is macroscopic haematuria, but patients are most susceptible post operatively if bladder irrigation is not sufficient; they suffer from clot retention within the catheter.
Treatment of the non operated patient is catheterisation with a three way catheter, with irrigation. In the post operative patient attempts should be made to mechanically free the clot.