Renal Flashcards
What are the main causes of CKD
Diabetes
Hypertension
Glomerular disease (including glomeruloneprhitis)
Polycystic disease
Recurrent UTIs
How would CKD present or end stage renal failure
- hypertension ( kidneys filtering ability decreases which means more fluid is retained leading to hypertension and oedema)
- breathlessness due to anaemia
-palpitations and muscle cramps from hyper kalemia
- fatigue and dizziness from less EPO
- bone pain from decreased vitamin D
- pruritus (from increases in urea)
The release of renin is controlled by what things
- changes in pressure at afferent arteriole
- sympathetic tone
- changes in chloride and osmotic concentration detected by the macula densa
- local prostaglandin release
What are the actions of angiotensin II
- systemic vasoconstriction to increase blood pressure (specifically the efferent arteriole
- increasing sodium and water retention
- also increases aldosterone secretion by the adrenal cortex
What is the effect of endothelin on kidneys
Inhibits sodium and water absorption
Antagonises the action of ADH and aldosterone
What is the effect of prostaglandins on the kidney
- causes vasodilation of the afferent arteriole increasing blood flow and GFR. Promotes diuresis
Nitric oxide works in a similar fashion to endothelis
How many stages are used to categorise CKD
5 stages
Stage 1 less than 90mL/min
Stage 3 split into 3a and 3b
Stage 5 less than 15mL/min
What is Fanconi syndrome
Disease affecting the PCT in which amino acids, bicarbonate, glucose, phosphate, proteins, and uric acid are not re absorbed leading to symptoms.
Can be inherited (mostly presents in children) or acquired later on in life in adults.
Acquired maybe due to drugs such as anti-virals, cisplatin or azathioprine
Red cell casts almost always diseased relating to which part of the nephron
Glomerulus
Features of nephrotic syndrome
Heavy proteinuria greater than 3.5g per day
Hypoalbuminaemia - leads to fluid overload and oedema
Hyperlipidaemia (increase in LDL +VLDL to compensate for lack of albumin as they are lipoproteins)
What things are included in the management of nephrotic syndrome
- fluid restriction and low salt (to reduce oedema)
- replacing lost albumin
- diuretic like furosemide to get rid of excess fluid
Consider:
- increase risked of thromboembolism as loss of anti thrombin in urine
- increased risk of sepsis as loss of immunoglobins - decreased immunity
Most common of nephrotic syndrome in children
Minimal change disease
What is the most common cause of AKI
- acute tubular necrosis
What are the 2 main causes of acute tubular necrosis
- ischaemia caused by sepsis or shock
- nephrotoxic substances such as aminoglycosides, myoglobin, radiocontrast agents and lead
What electrolytes changes are seen in ATN
Rise in urea, creatinine and potassium
What are the features of ADPKD
- hypertension
- recurrent uTIS
- flank pain
- haematuria
- Palpable kidneys
- Renal stones
Causes cysts in other organs such as the liver, spleen, pancreas.
May also cause berry aneurysms leading to subarachnoid haemorrhage
What is Alport’s syndrome
X linked genetic condition which leads to faulty formation of collagen in the glomerular basement membrane therefore leading to
microscopic haematuria
Progressive renal failure
What are the causes of AKI (pre-renal)
- hypovolemia secondary to diarrhoea or vomiting
- RA stenosis
Examples of renal causes of AKI
- glomeruloneprhtis
- ATN
- AIN
- rhabdomylosis
What are the post renal causes of AKI
- kidney stone
- BPH
- external compression of the ureter
Who is at increased risk of AKI
-previous AKI
- other failures (heart, diabetes)
- recent use of nephrotoxic drugs
- CKD
-use of iodine contrast agents
What meds should be stopped in AKI
- NSAIDS. - (decrease renal perfusion)
- aminoglycosides (
- ACEi and ARBS -decrease renal perfusion
- diuretics (decrease perfusion as lower blood pressure and volume)
What may have to stopped in AKI as there is risk of toxicity if it builds up
Metformin
Digoxin
Lithium
Hyperkalemia occurs in AKI. What is used to protect the myocardium
- calcium gluconate
- insulin and dextrose used to shift extraceullalr to inside.
- calcium resonium used to remove potassium from the body
What are the features of Good pastures syndrome
- causes pulmonary haemorrhage and rapidly progressive glomerulonephritis (blood and protein loss)
- more common in men
- associated with HLA DR2
What does renal biopsy show in GP syndrome
- linear IgG deposits along the basement membrane
What is focal segmental glomerulosclerosis
Presents as haematuria (microscopic), proteinuria, hypertension, xanthelasma. This progresses to nephrotic syndrome with significant loss of albumin and then ESRD
Investigated by light microscopy which demonstrates regions of scarring within the renal tissue. The deep corticomedullary glomeruli are affected first
Causes can be primary which is genetic or secondary due to pre-existing renal disease, SCD,HIV and lupus and use of heroin
On renal biopsy glomeruli may appear glassy
What diseases cause nephrotic syndrome:
Primary
- minimal change disease
- focal segmental glomerulosclerosis
- membranous glomerulonephritis
- membranoproliferative glomerulonephritis
What are the secondary causes of nephrotic syndrome
- diabetic nephropathy
- lupus nephritis
What are the complications of nephrotic syndrome
- thromboembolism - getting rid of anti-thrombin proteins
- microcytic hypochromic anaemia
- infections
What is the pathophysiology of diabetic nephropathy
- excess glucose in the blood causes glycation of the proteins which causes the basement membrane to thicken. (Hyaline arteriosclerosis)
This causes arteriole dilation to increase pressure and blood flow into the glomerulus) —> causes damage over time causing filtration slits to widen leading to loss of protein
What is the pathophysiology of FGS
- cause is unknown but it causes focal sclerosis of the glomerulus.
- foot processes of the podocytes become damaged.
- proteins, lipids trapped within the glomeruli - hyalinosis occurs
Secondary causes include SCD, HIV, renal hyerfiltration (only having 1 kidney)
What are the risk factors for FGS
Black african descent
Morbid obesity
CKD
What is the pathophysiology of membranous glomerulonephritis
Primary - idiopathic
Secondary: infections, neoplasms , drugs, hearty metal poisonings and autoimmune diseases (SLE, RA and Sjögren’s syndrome)
-leads to deposition of complexes at basement membrane (spike and dome pattern) triggers immune response which releases cytokines and inflammatory cells causing damage — leads to protein loss
What are the main risk factors for MCD
Hodgkins lymphoma
What are the functions of the kidneys
Elimination of metabolic waste
Water homeostasis
Electrolyte homeostasis
Acid base homeostasis
Blood pressure control
Vitamin D
Erythropoiesis
Renin
Excretion of drugs and metabolites
What parameters are used to measure renal function in AKI
1) serum creatinine. (Can be influenced by gender, ethnicity, age, body mass, diet and exercise)
2) urine output
EGFR is used in CKD. What is it based on
- creatinine, age, gender and ethnicity
Diagnostic criteria for CKD
EGFR of less than 60mL/min
Or
Kidney damage indicated by abnormal bloods, urine or imaging
Present for more than 3 months and tends to be irreversible
How many stages of CKD is there
5
Stage 5 (worst) = less than 15mL/min
CKD stages 3-5 increase with what
Age
Worse CKD staging also associated with lower SES
What are the risk factors for developing CKD
Increased age
Hypertension
Diabetes
Smoking
Poor education
Recurrent UTIs
Long term use of nephrotoxic meds
What systemic diseases cause CKD
Diabetes
Hypertension
What immune mediated diseases cause CKD
Membranous nephropathy
IgA nephropathy
SLE
Which infections can cause CKD
HIV
HBV
HCV
Tb
What genetic diseases can cause CKD
Polycystic kidneys
Cystinosis
Complications CKD
Cardiovascular disease (inappropriate elevation of blood pressure puts strain on the heart. Also unable to get rid of water - fluid overload increases blood Pressure,
more prone to atherosclerosis as dyslipidameia occurs)
Metabolic acidosis ( can’t excrete H+ and reasborb bicarbonate )
Uraemia (failure to excrete urea)
What diagnostic measures confirm AKI
Stage 1 — creatinine 50-100% increase from baseline and less than 0.5ml/kg/hr for 6 hours urine output
Stage 2 — creatinine 100-200% increase from baseline and less than 0.5ml/kg/hr for 12 hours
Stage 3 — >200% increase. <0.3ml/kg/hr for 24 hours
What meds increase risk of AKI
Diuretics
Acei arbs
NSAID
Gentamicin
Vancomycin
Chemo
Diagnostic criteria for nephrotic syndrome
Proteinuria - more than 3g
Peripheral oedema
Hyperlipidaemia
What are the primary diseases causing nephrotic syndrome
FSGS
Minimal change disease
Membranous nephropathy
Damage to filtration barrier occurs leading to protein leak
What are the secondary causes of nephrotic syndrome
DM
Cancers
Drugs
Infections
SLE
Amyloidosis
What are the complications of nephrotic syndrome
Thromboembolism
DVT and PE
Infection
Hyperlipidaemia
AKI
CKD
Treatment of nephrotic syndrome
- diuretics
- salt restriction
- reduce proteinuria by acei and arb
- thromboprolylaxis
Diagnostic criteria for nephritic syndrome
Proteinuria less than 3g
Haematuria
Hypertension
Oedema
AKI/ckd
What are the causes of nephritic syndrome
Usually inflammatory or immune mediated
- autoimmune
SLE
ANCA vasculitis
Anti-glomerular basement membrane antibody disease
Infection related:
Post infectious glomerulonephritis
Bacterial endocarditis
HCV
What is the surgical triad which causes most AKIs in hospital
Post operative volume depletion
Infection
Nephrotoxic drugs
What % of akis are caused by parenchyma damage
Less than 5%
Post renal 10%
Which groups are at risk for AKIs
Elderly
Diabetics
Vasculopaths
Chronic renal impairment
Chronic liver disease
Cardiac dysfunction
What kind of drugs can impact the function of the kidneys
ACEI + ARBS
NSAIDS
PPIs cause interstitial nephritis
Aminoglycosides
Contrast medium
Remember a normal serum creatinine is not synonymous with a normal GFR
What are the life threatening complications of AKI
Hyperkalemia
Pulmonary oedema
Uraemic encephalopathy
Pericardial fluid
Who is involved in MDT of renal patients
Nephrologist
Dietician
Transplant nurse
Dialysis technician
Clinical pharmacist
Community peritoneal dialysis staff
Haemodialysis staff
Surgeon
Where does urea come from
Proteins are broken down into amino acids which are converted to ammonia which is very toxic so it is converted to urea. Conversion occurs in the liver but urea is excreted via the kidneys
What test is used to measure urea levels
BUN blood urea nitrogen
What is oliguria
Volume of urine below which body cannot excrete products of metabolism
Why might acutely sick patient in AKI become acidotic
Failure to remove acid from the body via H+ excretion
Production of other acids such as lactic acid from tissue hypoxia
What ECG changes occur in Hyperkalemia
Tall tented T waves
Wide WRS and disappearance of P wave
Sine waves
What methods are used to assess intravasular volume
Body weight
Skin turgor
Postural blood pressure
Mucous membranes
JVP
Lung bases
What complications occur in CKD
Anaemia
Renal bone disease (Vit D)
Acidosis
Hypertension (fluid overload
Malnutrition
Uraemia
What can cause haematuria
Infections - carry out urine microscopy and culture
Renal stones:
Urothelial malignancies
BPH or strictures
What does absolute anuria mean
Urinary tract obstruction
What happens in Fanconi’s anaemia in relation to the bone marrow vs Fanconi syndrome
Anaemia - Type of bone marrow failure in which DNA repair machinery is faulty leading to pancytopenia.
Syndrome : Significant renal involvement occurs in which the PCT is not able to re absorb required electrolytes and substances
What classification is used to assess the severity of AKI
RIFLE
Risk
Injury
Failure
Sustained loss
End stage renal disease
What are examples of true and relative hypovolemia
True -
GI (diarrhoea and vomiting)
Burns
Haemorrhage
Relative
Heart failure
Septic shock
Hepatorenal failure
What are the clues to renovascular disease
Atherosclerotic disease elsewhere
Hypertension
Vascular bruits on examination abdominal
What parts of the nephron may be affected in renal disease
Glomeruli
Tubules
Intersitium
Blood vessels
What diseases can impact tubular function
Ischaemic ATN
Nephrotoxic ATN
Intratubular obstruction like crystals, myoglobin and myeloma
What can impact the interstitum in terms of renal causes of AKI
Acute pyelonephritis
Acute interstitial nephritis (infection or drugs)
What can impact the vascular compartment in terms of renal causes of AKI
Vasomotor drugs that reduce perfusion to the kidneys
Malignant hypertension
Vasculitis
Micro vascular obstruction like an emboli
Microalbuminuria is associated with what conditio
Early diabetic nephropathy
- can be measured via albumin: creatinine ratio
Urine dipstick will be negative
Visible haematuria indicates bleeding within the urinary tract whilst microscopic haematuria indicates..
Glomerular haematuria
What kind of things can cause obstruction
Tumours
Stones
Prostatic hypertrophy
In urethra tumours, valves (in young boys congenital condition), strictures and foreign bodies
What are the signs and symptoms of uraemia
Anorexia
N+V
Pruritus
Neuropathy
Pericarditis
Confusion
Encephalopathy
Coma
Impact of kidney failure on other body systems
Causes hypertension and left ventricular hypertrophy
Peripheral oedema
Pulmonary oedema
How does renal failure cause bone disease
Decreased D3 means that less calcium is absorbed. This triggers PTH which causes resorption of bone to release calcium into the blood — this may lead to vascular calcification
Increased. Phosphate triggers PTH release. — renal osteodystrophy
What is renal osteodystrophy
Due to low levels of calcium and vitamin d and other altered electrolytes there is changes to bone mineralisation leading to bone pain and pathological fractures
Signs of low calcium also occur (abdominal pain, cramp, seizures)
Chovsteks sign
Trousseaus
What is the treatment of chronic Hyperkalemia
Loop diuretics flush out potassium
Consider dietary potassium restriction
How is acidosis treated in ckd
Sodium bicarbonate
What ECG changes are seen in Hyperkalemia
Tall tented T waves
Wide QRS
Absent p waves
Sine waves
What are the advantages of renal transplant
- don’t need dialysis lifelong
- improves renal clearance
- restores endocrine functions of the kidney
- improves LE
Disadvantages of renal transplants
Perioperative mortality risk (CV mortality)
Lifelong immunosuppression
Cancer risk for lymphoma
New onset post transplant diabetes
What are the contraindications for renal transplant
Active infections
Active cancer
Active drug misuse
Uncontrolled major psychiatric disease
Non concordance with treatment
Short LE <5yr
What is tissue typing (HLA compatibility)
All cells in the body have antigens that allows the body’s immune system to differentiate its own cells from non self or foreign. If a tissue is introduced that will trigger an antibody response. Antigen is presented to T cell by antigen presenting cells ( class II MHC molecules and co-stimulatory molecules). This T cell will then undergo IL-2 mediated clonal expansion and recruit other immunoreactive cells
In this test the recipient is tested to see whether they have antibodies against the antigens on the donors tissue/organ
For renal transplant ABO blood group must match as well
What kind of drugs are used to prevent rejection following transplant
Calcineurin inhibitors
MTOR inhibitors
Anti-metabolites
Monoclonal antibodies
Steroids
Mechanism of hyper acute rejection
When recipeient has pre-formed antibodies to donor kidney
Complement activation and infmamotyr cell infiltration results in endothelial damage
What occurs in acute rejection
Antigen is presented to T cell — clonal proliferation
T helper recruit cytotoxic T cells — cellular toxicity
B cells produce donor specific antibodies
Examples of calcineurin inhibitors and how they work to prevent organ rejection
Cyclosporine
Tacrolimus
Inhibit calcineurin which is an enzyme required for the activation of T cells .
Inhibiting calcineurin leads to decreased production for IL-2 which is required for clonal expansion of T cells
How does sirolimus work
Inhibits MTOR pathway which is needed for cell cycle in T cells
Also affects B cells
Blocks response of T cells to IL-2
How does azathioprine work
Is a pro drug which must be activated into 6 mercaptopurine
Inhibits the synthesis of purines A+G which are needed for DNA synthesis. This prevents the cells from dividing and prevents T and B cell proliferation
How does mycophenolic acid work
Blocks IMPDH enzyme responsible for purine synthesis. Cell cannot divide with DNA replication and synthesis.
B and T cells cannot proliferate
How does leflunomide work
Inhibits DHODH enzyme which is responsible for synthesis of pyrimdines. Cell cycle cannot progress
b and T cells can’t proliferate
Mechanism of action of alemtuzunab
Monoclonal antibody binds to glycoprotein CD52 on surface of immune cells triggering self destruction of these cells
Mechanism of action of basiliximab
Monoclonal antibody which binds to CD25 part of IL-2 receptor thus preventing IL-2 from binding.
IL-2 is required for clonal expansion of T cells
What is the treatment of FSGS
- immunosuppressants - pred
- dietary restriction of salt.
Post strep glomerulonephritis presentations and diagnostic test
- headache
- sore throat
- non-specific joint pain
- hypertension
- haematuria
- renal biopsy is the diagnostic test
Fever can cause hypotension
- causes vasodilation which reduces blood pressure
- also through sweating which causes fluid loss — lower BP
Losses:
Sensible: loss of fluid from tubes within the body (can be measured)
( vomiting, urine output, diarrhoea + blood)
Insensible ( sweating and breathing (mouth - lose water)
Sepsis can cause intrinsic renal failure: T or F
True
Specific gravity will be raised in pre - renal failure T or F
T
As the urine is more concentrated (more solutes)
Causes of anaemia 3 Hs
H - haematopeeitic - can’t make red cells ( deficiencies, CKD, malabsorption, BM failures)
H - haemolytic - breaking down of the red cell
H aemorrhagic - loss of blood cell
ACEi in acute vs chronic renal failure
Nephrotoxic in acute
Protective in chronic renal failure
Management of Hyperkalemia FAR
F - force potassium into cells (takes seconds to minutes)
( glucose with insulin) 10ml of 10% of glucose with 10 units of insulin
(Sodium bicarbonate )
B2 agonist - salbutamol (IV or nebs)
Antagonise potassium on cells: hours
- calcium gluconate IV
Remove K from blood:
- dialysis
- Na/ Ca resonium suppository
What are the 4 acute life threatening complications of CKD
1) Hyperkalemia
2) hyperphosphatemia
3) fluid overload
4) uraemic encephalopathy
Management of hyper phosphate
Phosphate binders ( calcium acetate)
Treatment of fluid overload
- consider ventilation
- consider therapy for hypertension
Renal dialysis
Treatment for uraemic encephalopathy
- dialysis
What form of heart failure do patients with chronic renal failure develop
Concentric left ventricular hypertrophy
Sub endocardial region is not well perfused due to thickened ventricular wall. So more susceptible to MI in this region - non ST elevation presentation
Muscle is not relaxing very well during diastole leading to hypo-perfusion
Radio-femoral delay is indicative of what disease
Coarctation of the aorta:
Tear in the intima of the aorta - blood separates into two - radial artery gets blood earlier
ACEi and ARBS are absolutely contraindicated in what condition
Renal artery stenosis
What are the contraindications for dialysis
No absolute
Do consider age, cause of ESRD, prognosis….
Indications for urgent dialysis
Pericarditis
Uraemic encelopathy
Fluid overload unresponsive to diuretics
Poorly controlled hypertension despite treatment
Persistent metabolic disturbances despite treatment
What is the difference between haemodialysis and haemofiltration
- haemofiltration occurs in patients who are not cardiovascularlly stable
- haemodialysis - diffusion - better at acid base issues
- haemofiltration - convection - better at water + solute issues
Contraindications to renal transplant:
Contraindications to surgery —- CVD, morbid obesity, hepatic disease, CJD
To immunosuppression: aucte infection, malignancy, HIV
Recurrent renal disease:
- IgA nephropathy
- diabetic nephropathy
- hereditary oxalosis
- substance abuse
What is the effect of PPIs on the kidneys
Can cause acute interstitial nephritis
What is normal GFR
120ml/min
Diabetic nephropathy pathology
Increased blood sugars increases tonicity of the fluid which results in greater flow through the glomerulus — increased pressure and constant stretching of the glomerulus causes slits in membrane to become wider — proteinuria
PCR & ACR
- acr better measure in diabetes as albumin is more affected
What are the issues with SGLT-2 inhibitors
Glycosuria increases risk of infections
Normoglycaemic ketosis
How do GLP1 agonists work
Incretin hormones like GLP-1 and GIP stimulate the release of insulin after glucose intake.
Inhibit release of glucagon
Delay gastric emptying and
Increase glucose uptake from muscles
Decrease glucose production in the liver
Hypertensive renal disease
Intimal thickening of small vessels
Onion skin large vessels
Kidneys become smaller
Glomerulosclerosis
Fibrinoid necrosis
Side effects of ACEi
Hyperkalemia
Dry cough
Manifestations of nephritic syndrome
Haematuria
Uraemia
Hypertension
Hyperlipidaemia
Types of vasculitis
*** add notes
Types of vasculitis
*** add notes
P - ANCA test for..
Small vessel vasculitis
C -ANCA
Large vessel vasculitis
HUS
Occurs in children under 10 mostly after shiga toxin producing E.coli infection
Shiga toxin - release of inflammatory cytokines which causes vascular injury leading to formation of microthrombi
Enters cell and binds to ribosome causing destruction of the cell.
Microthrombi and damaged Rbc become stuck in glomerulus — complement activated — renal damage and necrosis
Presents as bloody diarrhoea, abdominal pain and vomiting and fever. + oliguria and oedema + bruising
TTP thrombotic thrombocytopenic purpura
Blood clots form in small vessels which might block blood flow to major organs.
This is caused by deficiecies or changes to an enzyme which controls the blot clotting process
Genetic
Acquired: can be caused by drugs like chemo. Cancer, HIV, lupus may trigger this
More common in women
Antibodies in SLE
ANA - general
Anti double stranded DNA - more specific
What is plasmapheresis
What is the presentation of IgA nephropathy: Berger’s disease
Caused by abnormal activation of the immune system which results in deposition of igA complexes in the kidneys.
This then triggers complement cascade C3 or C4 which causes damage leading to haematuria, hypertension and proteinuria
Usually after an infection like URTI, or gastroenteritis
Is the most common cause of glomerulonephritis in adults
Characteristics of post infection glomerulonephritis
Haematuria
Ödema
Hypertension
Proteinuria
Occurs mostly in children 1-2 weeks after strep throat
Presence of immune complexes causes complement activation which causes damage to the glomerulus leading to symptoms of nephritic syndrome
On microsocopy there is subepithelial humps which are electron dense deposits near the BM.
IgG and C3 deposits are found on microscopy
what are the characteristics of membranoproliferative glomerulonephritis
Has features of both nephritic and nephrotic syndrome
mesangial cells proliferate + immune deposition in the sub-endothelial space
What is the presentation and pathology of ANCA gomerlonephritis
Haematuria,
Proteinuria
Hypertension
Oedema
Autoimmune condition in which antibodies released by plasma cells activate neutrophils to release granules wich cause damage to the glomerulus — inflammation, fibrosis and scarring occurs leading to renal impairment
Examples of large vessel vasculitis
1) giant cell arteritis
Affects large arteries specifically temporal artery
Causes headaches, jaw pain, vision probs, fatigue
Examples of medium vessel vasculitis
1) polyarteritis nodosa
Mostly affects skin, kidneys, nerves and GI system. Causing muscle pain, fatigue, weight loss, nerve damage leading loss of sensation and abdominal pain
Associated with Hep B + C
2) kawasakis disease - children
Especially affects coronary arteries (complications is CA aneurysm if untreated)
High fever, strawberry tongue, swollen hands,feet and lymph nodes
Examples of small vessel vasculitis
1) granulomatosis with polyangitis (wegeners)
Affects. Arterioles, venules and capillaries in which grnaulomas form.
Typically affects resp tract: chronic sinusitis, nosebleeds, cough, haematuria, SOB
Affects bilaterally represented organs
Associated with C-ANCA
2) microscopic polyangitis
Kidneys and lungs affected. Haemoptysis + haematuria, proteinuria, fever + weight loss
Associated with P-ANCA
3) churg-Strauss syndrome (eosinophilic granulomatosis with polyangitis)
Only affects individual with asthma or allergic rhinitis
Associated with p-ANCA
4) henoch schonlein Purpura / IgA vasculitis
Deposition of igA
What causes variable vessel vasculitis
BEHCETS disease
Painful oral and genital ulcers, uveitis, skin lesions etc
What is MPGN type I
Damage occurs as immune complexes and C3 proteins are deposited in subendothelial space
Associated with chronic infections, SLE and multiple myeloma
What is MPGN type II
No immune complexes deposition occurs. Abnormal activation of complement causes glomerular damage causing both nephritic and nephrotic syndrome symptoms
what causes the production of struvite stones
caused by GR-ve urease producing bacteria that convert urea to ammonia.
pseudomonas
proteus
klebsiella
what are the risk factors for urolithiasis
= anatomical variations that lead to stasis
= low urine volume
= recurrent UTIs
= meds - anti virals
= hyperparathyroid, metabolic syndrome, gout,
= acidic urine (increased protein intake)
= genetic disorders affecting cysteine metabolism
