c
 


 

   

  
Low potassium <3.5mmol/L, most common electrolyte disorder usually due to diuretic
therapy.
It can occur due to increased loses in GI/ GU tract (Diarrhoea, vomiting, laxative abuse)
decreased intake or a shift to the intracellular component.
Renal loses ʹ diuretics, mineralocorticoids excess (conn͛s syndrome, Cushing͛s syndrome,
ectopic ACTH, secondary hyperaldosteronism [renal artery stenosis, hypertension and heart
failure], renal tubular acidosis.
Beta-receptor stimulation causes hypokalaemia

Clinical features
à| £ften asymptomatic
à| ºeakness, intestinal ileus,
à| ÑCG ʹ T wave flattening, appearance of U waves and increased incidence of
tachyarrhythmia͛s
Long standing hypokalaemia can lead to poorly reversible damage of the distal tubule,
leading to a failure of renal concentrating properties ʹ polyuria and polydipsia
Replace with IV potassium infusion or oral supplements.

   
The main cause for this is renal failure, but it can also occur with Addison͛s disease,
spironolactone, ACÑi and potassium retaining diuretics such as amiloride.
Cell destruction ʹ haemolysis/ chemotherapy and rhabdomyolysis can liberate large
amounts of potassium.

Clinical features
à| Usually asymptomatic when severe can cause muscle weakness|
à| ÑCG ʹ Peaked T-waves, QRS widening, prolonged PR, loss of P waves|
|
Management
If the potassium is less than 6 then it should be managed by restricting intake, however
greater than 6.5 or in the presence of ÑCG changes this should be viewed as a medical
emergency.
v|

  
 this stabilises the myocardium
v|
 

 





v| þ 

v| 



 
£ccurs when sodium drops below 130 ʹ often asymptomatic but can cause nausea,
vomiting, muscle cramps/ weakness, confusion, coma and convulsions.

1.| Hypovolaemia ʹ where the patient is both water and sodium deficient
Renal losses: high urinary sodium occurring in Diuretics, Salt loosing nephropathy and
Addison͛s
Ñxtra-renal: occurring in vomiting, diarrhoea, burns and sweating.
2.| Normovolaemia ʹ modest increase in water causing a relative Hyponatraemia
Inappropriate IV fluids (e.g. 5% dextrose)
SIADH
Sickle cell syndrome
3.| Hypervolaemia ʹ increase in sodium and water
Cardiac failure
Hepatic failure
Nephrotic syndrome
Inappropriate IV fluids (normal saline)
c
 



Management
Seek to identify and manage the underlying cause and determine the patient͛s volume
status. If the patient is hypovolaemic then administer IV saline. As Hyponatraemia can also
occur in normo/hypervolaemia if the patients volume status is normal and they are
symptomatic then restrict their oral intake. In patients with hypervolaemia (oedema, HTN,
JVP) then fluid restriction and diuretic therapy may be needed.

In chronic hyponatraemia rapid correction can cause 






;
encephalopathy, cranial nerve palsies and quadriplegia.

Syndrome of Inappropriate ADH secretion

Relatively common in hospital patients but requires the exclusion of adrenal, thyroid,
pituitary and renal insufficiency, in patients who are euvolaemic and not on diuretic therapy.
This leads to increased ADH
Causes;  

 
 !
 "      



!
 # 
!$

 

%
Management involves removing the cause and fluid restriction, failing this   


blocks the effects of ADH.

 
 
Sodium greater than 145, caused by a relative water deficit, and occurs in patients who are
unable to increase their water tolerance.

1.| Hypovolaemia
Renal losses: Diuretics, post obstruction, osmotic diuresis
Ñxtra-renal losses: Sweating, burns, diarrhoea, and fistula
2.| Normovolaemia
Renal losses: Diabetes insipidus, impaired thirst
Ñxtra renal losses: Insensible loss from skin, respiratory loss
3.| Hypervolaemia
NACL
Hypertonic dialysis
Cushing͛s syndrome
Hyper aldosteronism

As before it is essential to determine the patients volume status and determination of

urinary sodium
Common causes:
ºater deprivation particularly in elderly people, and hyperosmolar diabetic coma

Management
Identify and correct the underlying cause, in those with Hypovolaemia administer IV saline.
In hypervolaemic hypernatraemia the excess sodium must be removed ʹ diuretics
ºhen patients are euvolaemic then administer 5% dextrose.

Diabetes Insipidus
This results in polyuria and polydipsia and occurs due to defects in ADH secretion

h& !
 
 !h
The presence of severe acidosis requires immediate diagnosis and treatment; there are 4
main categories.
1.| Ingestion of acids: salicyclate, methanol
2.| Accumulation of endogenous acids: lactic acid in tissue hypoperfusion, ketones DKA
3.| Loss of alkali: severe diarrhoea, biliary or enteric fistula, or in proximal renal tubular
acidosis
4.| Failure to eliminate acid: Renal failure, distal tubular acidosis
The anion gap is normally 12 +- 2, if it is elevated it indicated the presence of additional
acids; DKA, lactate, and if it is low suggests the loss of alkali.

 

  
 
 

 
!!
 '


    (

Lactic Acidosis
This can be divided into 3 categories. Increased production, which occurs in any form of
tissue hypoperfusion / hypoxia, status epilepticus and marathon runners, destruction of
large tumour masses and in poisoning ʹ C£, cyanide
If there is cardiac failure then lactate will not be shifted effectively, and any liver failure will
interfere with its metabolism
 !h 
This is usually asymptomatic.
Usually this is caused by loss of acids ʹ vomiting eg pyloric stenosis, but can occur due to
increased renal re-absorption; hyperaldosteronism, hypokalaemia
There may be a respiratory compensation with a fall in respiratory rate.

c 
h
Reduced ventilatory rate may cause an acidosis through the accumulation of carbon dioxide
Causes
à| Sedation: opiates
à| Respiratory Muscle weakness: GBS, Polio, MG
à| C£PD
Hypercarbia may present clinically with a bounding pulse, papilloedema and a metabolic
flap. If this is longstanding there may be a rise in bicarbonate level due to renal
compensation.

c 
h 
Increased ventilation ʹ fall in pH which occurs in response to hypoxaemia, panic attacks or
excessive artificial ventilation and stimulation of respiration by CNS drugs or pulmonary
disease.
This is associated with a fall in ionised calcium ʹ Paraesthesia, light-headedness and
carpopedal spasm, tetany can occur in severe cases
c
þ
Common condition occurring in 2% of the population, mainly affecting men in their 30-40s.
Most stones are made of ) , the remainder are ) 


 (usually caused by infection),  


)


(

Stones usually form when there is a high serum calcium level ʹ which can occur in
hyperparathyroidism, Sarcoidosis and myeloma. This can then pass into the urine, especially
in immobile patients, or those with renal tubular acidosis or cushings syndrome. ºhen these
solutes exceed their solubility stones precipitate, this can also occur with  
*+ (

Clinical features
à| Haematuria ʹ microscopic and macroscopic
à| Loin pain, renal coli, supra pubic pain
à| Dysuria
à| UTI
à| £bstruction
à| Acute on chronic renal failure

Investigations
&þ ʹ exclude haematological malignancies, *,-'
 
.
 
ʹ urate, calcium, oxalate and citrate
/*

* *//
h cʹ demonstrate position and rule out obstruction

v| Prevention consists of increasing endogenous inhibitors of stone formation by giving

oral potassium citrate, lemon juice and avoiding a low potassium diet.
v| Prophylactic antibiotics may prevent recurrent UTI͛s
v| Thiazide diuretics/ low protein diet
v| Allopurinol if oxalate stones or grout ʹ and reduce dietary oxalate (rhubarb and
spinach)
v| Phosphate stones ʹ acidify urine
v| £xalate ʹ increase B6
v| Cystinuria ʹ alkalisation
 

 0 /

 
Kidneys normally excrete about 150mg of protein a day and this constitutes glycoprotein
secreted by the tubular cells. Higher amounts of protein indicate renal disease often
glomerulonephritis.
Dipsticks are designed to test for albumin, they will not detect "
, which occur in
myeloma (Bence-Jones) or microalbuminuria, which is an early sign of diabetic nephropathy.
à| Serum urea and creatinine
à| 24hr urine ʹ total creatinine clearance and total protein excretion
If these confirm the presence of significant Proteinuria:
à| USS of renal tract
à| Blood glucose to exclude DM
à| Immunological investigation to exclude myeloma, SLÑ or systemic Vasculitis (ANA
and ANCA)
à| In severe >2g proteinuria ʹ c
&

1   
2.(
.
   0 /

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0 /

 
1.| Proteinuria
2.| Hypoalbuminaemia (<30g/Dl)
3.| Peripheral oedema
Haematuria is rare and BP is usually normal.
There are many causes of nephrotic syndrome ʹ the most common is glomerular disease:
GN: 

 (most likely cause in children),  !




 
  (Following glomerular disease !   
h

(primary/ secondary or multiple myeloma),  and other causes such as /1-(

There may be many complications of nephrotic syndrome such as oedema,
hypercoagulability (which may lead to renal vein thrombosis and DVT),
hypercholesterolemia, and infection (Therefore is it recommended that all patients have
pneumococcal vaccine)

Treatment
Management is initially directed at the underlying cause if identified.
à| Diuretic therapy ʹ cautiously as Hypovolaemia will worsen renal disease
à| ACÑi reduces proteinuria and HTN
à| Statins
à| Anticoagulation only when required

+ 0 /

 
This differs in that there is heamaturia, usually microscopic and mild proteinuria not
substantial enough to cause a nephrotic syndrome. The kidneys can͛t excrete fluids ʹ HTN,
oedema and oligouria. Due to the decreased GFR patients may become uraemic
Commonly associated following group A beta- haemolytic step, 2-3 weeks later. The
differential diagnosis is substantial.
h c
 
v| Asymptomatic
v| £ligouria <400mls/ 24hrs
v| Raised creatinine and urea

Normal people should have a urine output of 30mls or less.

Pre-renal causes
/  
  
 v
 


hþ-3
 



Any of these can then induce h +!0 .

Renal causes
"0  h 
 
 
v
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Post-renal causes
&


 
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Management
à| Take a careful history including a detailed medication history ʹ baseline
biochemistry and urine dipstick.
à| Check calcium and uric acid levels
à| Perform a PR/ PV
à| USS renal tract
à| Antibodies ʹ ANCA for Vasculitis, AGBM ʹ good pastures and ANA for SLÑ
à| Renal biopsy

The overall aim is to treat the underlying cause. Loop diuretic therapy may be used, along
with relief of any obstruction. It is very important to monitor the U&Ñs, fluid balance and
weight of patient with AKI. If patients are oligouric/ anuric they will need fluid restriction.
£ther general measures include ʹ low protein diet.

Absolute indications for Renal Replacement Therapy

1.| Hyperkalaemia
2.| Creatinine >1000
3.| Severe acidosis
4.| Fluid overload ʹ pulmonary oedema.
þ
c
 

1.| Diabetic Nephropathy
2.| Chronic GN
3.| Vascular disease ʹ +0'c
v 
4.| PKD

Clinical features
These can be fairly non-specific
à| Lethargy/ fatigue and malaise
à| Generalised pruitus ʹ excoriations
à| Restless leg syndrome
à| Impotence
à| Menstrual irregularity
à| Sub-fertility

Important signs on examination include pallor/ colour, HTN, oedema and peripheral
neuropathy and proximal myopathy

Investigations
U&Ñs ʹ raised urea and creatinine (not sensitive), hyperkalaemia and reduced phosphate
LFT͛s ʹ raised ALP
FBC ʹ anaemia ʹ responds well to - 
þ 

 
 ʹ slightly overestimates GFR
.v
 

h c c
+*// c
&


Management
The aims here are to slow the decline of renal disease preserving GFR, and to treat any
complications ʹ bone disease, cardio-vascular disease and anaemia

Lifestyle must be addressed ʹ in particular  , it is important to maintain a low protein, low

potassium diet. Patient also benefit from 
 
.
In addition 
 



  must be aggressively treated.

Renal replacement therapy should be discussed in advance and started when GFR falls
below 10ml/min.

!  
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v| þ
 


  are nephrotoxic.
v| h

  )

/

 can also accumulate in renal disease.
v| Caution is advised with hþ- (renal artery stenosis ʹ check U&Ñs 2 weeks after
starting) and 0/h which can cause fluid retention and worsen GFR
v|  are also less effective in renal disease

ABS£LUTÑLY C£NTRAINDICATÑD
1.| Potassium sparing diuretics
2.| Metformin
3.| Tetracycline
" 

Presents with one of more features of renal disease
v|    
v| Proteinuria
v| HTN
v| Nephrotic Syndrome
v| Renal failure

C£NTRAINDICATI£NS T£ RÑNAL BI£PSY

1.| £nly 1 functioning kidney
2.| Small kidneys
3.| HTN
4.| Bleeding disorder

There are different classes of GN, ' (number of glomeruli affected),  
'
! (how much of the glomeruli is affected) and   
 
 (

IgA nephropathy ʹ Berger͛s disease
Commonest form of GN, which occurs in young males causing haematuria following
pharyngitis. 20% will progress to renal failure

HSP
This is a systemic variant of the above disorder. It presents with a 
v of the large
joints,  on the extensor surfaces and !

. Half of all patients
will go into remission, with 20% suffering some renal impairment and 5% progressing to
renal failure

Membranous Nephropathy
+  4


 . It is also associated with  






. It can present with any feature of renal disease and around
10% will go into Ñnd Stage Renal Failure within 5yrs.

Thin membrane Nephropathy

Persistent haematuria, normal BP and Renal function tests, positive FH

Membranoproliferative GN
There are two types, and it may be associated with 
 
 -
 & 


/1-(50% of patients progress to end stage renal disease within 10 years.

Minimal change Nephropathy

Fusion of the podocytes. This accounts for 5
4



 ( Associated with allergy and Hodgkin͛s lymphoma.

Systemic Vasculitis
Necrotising inflammation of the blood vessels, which can affect any organ, commonly the
kidneys in 6 
7. 90% remission with cyclophosphamide and Prednisolone.

Anti Glomerular Basement Membrane ʹ Good-pastures syndrome

Acute renal failure due to a rapidly progressive GN causes AKI. Can be associated with
pulmonary haemorrhage and S£B particularly in smokers ʹ responds to plasma exchange

SLÑ
Renal disease occurs in 90% of patients with SLÑ, steroids in combination with either
cyclophosphamide or Aziothiaprine slow progression.

Post- streptococcal GN
This occurs 2-3 weeks after a group B haemolytic strep infection; therefore take throat
cultures if the patient hasn͛t been treated with penicillin͛s.


c
c  
+ 

Indications
1.| Uraemia (anorexia/ lethargy ƒ N/V, bone pain, itch, S£B and seizures ƒ coma)
2.| Life threatening complications
v| Hyperkalaemia
v| Fluid £verload
v| Acidosis
v| Uraemic pericarditis
v| Ñncephalopathy

Haemodialysis
This is done through an AV fistula or a double lumen line. It involves the exchange of solute
though a semi-permeable membrane with blood and dialysate flowing counter-current.
This method is suitable for most people and is more effective than CAPD.

Drawbacks
à| Haemodynamic instability due to rapid fluid shift esp. in those with pre-existing CVS
disease
à| Hypotension
à| Disequilibrium syndrome
à| Requires vascular access ʹ bleeding, thrombosis, infection
à| Very inconvenient

Haemofiltration
Blood is filtered across a highly permeable membrane and the ultra-filtrate is then
substituted, therefore there is no need for a dialysate.
This causes less haemodynamic instability, but it more expensive.

Peritoneal Dialysis ʹ CAPD

This uses the peritoneum as a semi-permeable barrier, and several bags of isotonic or
hypertonic (glucose to remove excess fluid) solution as a dialysate. This requires a
+
   . The advantages of this method are that it is cheap, easier and can be
performed at home.

Drawbacks
à| Peritonitis
à| Catheter malfunction
à| Hernia
à| Low back pain
à| 1  

 .
c
+




C£NTRAINDICATI£NS
1.| Recent/ Current infection
2.| Age >70yrs
3.| HIV
4.| Severe heart disease
5.| Cancer
6.| Severe renal disease with a   
 

Kidney transplants can either with live (related and unrelated) or cadaveric. A HLA identical
live transplant will last around 20years compared to 8years for a cadaveric one.

Complications
   8Bleeding, thrombus, infection, urinary leak and oligouria
c 9 
8 This can be acute occurring before 6 months, which may respond to pulsed
methy-prednisolone, or chronic if it occurs after 6 months, which does not respond to
steroids.

 






The latter two complications occur secondary to long-term immunosuppression.

Rena transplants are cheaper, reduce mortality from renal disease and its complications.
However it is major surgery followed by life long immunosuppression with a 5 ʹ 10% risk of
failure.



:

  

Dominant disorder, with 25% occurring as spontaneous mutations. There are 2 PKD genes,
one on chromosome 16 and the other on 4. PKD is a multisystem disease and can also affect

      
 

Risk factors/ Increased incidence
à| Cardiac valve disease
à| Berry aneurysm ʹ History of subarachnoid haemorrhage
à| Hernias
à| Diverticular disease

Clinical features
Patients present with +0 !

 þc. Patients with this disease
usually progress to renal failure and will require RRT.

The diagnosis is made by ultrasound. Following this other family members can be screened/
given genetic counselling. Patients are not normally tested until they are 18 when the cysts
will be visible, can be done sooner if there is significant renal impairment.
c
þ þ

Usually adenocarcinoma ʹ occurring more commonly in men 65- 75yrs. These tumours may
be associated with a Paraneoplastic syndrome.
v| Hypercalcaemia
v| HTN
v| Polycythaemia
Usually occur in the upper pole and metastasise to the local nodes, bone, lung and liver.

Clinical features
May present with the classic triad of   


! (

Usually associated with a poor prognosis due to late presentation.
à| 30% present with metastasis and are inoperable
à| 30% present with Paraneoplastic syndrome
à| Left sided varicocele can occur in men
à| IVC obstruction ʹ bilateral leg swelling.

Investigations
Urine dipstick ʹ blood
USS ʹ mass
CT ʹ stages
Radio-nucleotide scanning ʹ bone mets

Management
c
 
also removes the perinephric fat, adrenal glands, upper ureter and
local nodes

 
if one functioning kidney, decreased renal function or bilateral cancer
h  !
if patients are unsuitable for surgery.

Prognosis is 70% if there are no mets but 15 ʹ 20% if there are. Late recurrence is common.