renal Flashcards
what are the different types of renal stones
Calcium oxalate, 65%
Calcium phoshphate 20%
Uric acid 10%
epidemiology and prevalence of renal stones
lifetime risk 10-15% age 20-40 is peak
Risk factors of stone formation
Dehydration - largest risk factor pre existing kidney disease PCKD UTI- Proteus Urinary factors - Hypercalcemia thiazide= increase uric acid
Prevention of stone formation
Overhydration reduce salt and sodium normal dairy moderate protein reduce BMI
where can stones form
upper, renal pelvis or ureter
lower bladder urethra prostate
Presentation of renal stones
Majority asymptomatic renal colic (associated with nausea and vomiting) Pallor sweating haematuria Auria UTI symptoms, voiding symptoms no signs on examination ( look out for gout tophi as a sign of excess uric acid
what is renal colic
severe abd pain, loin to groin
sudden onset
radiates to ipsilateral testicle or labia
writhing pain, unable to find comfortable position
colicky pain
pain usually subsited after a few hours
made worse by exercise or diuretics or alcohol
Investigations and diagnoses of renal stones
Before starting investigations start on Analgesia and antiemetics to stabilize patent
Non contrast CT of kidney ureter and bladder NCCT-KUB - diagnostic of stone
identify cause of stone: Bloods, Serum Ca, Serum uric acid. U and E. MC and S of MSU
differential diagnoses for patient present with renal colic
AAA
Gynae causes, Torsion of ovaries or ruptured ectopic
MSK
Torsion
Management of renal stones
Include preventative measures
Analgesia, NSAIDs, antiemetics
potentially give IV fluid if you want them to pass the stone
watch for sepsis
if stone <1 cm then conservative (hydrain, pain and antiemetic)
stone =2-3cm then lithotripsy (Extracorporeal shock wave lithotripsy)
stone >2cm Ureteroscopic laser
ureteric stent
Prevention of further if hypercalciuria ( thiazide if hyperuricemia (allopurinol)
trimethoprim or gentamycin
Complication of Renal stones
can cause sepsis
obstruction of UT can cause dilation and dilation of the kidney is hydronephrosis. if there was an infection present it could cause pyonephrosis
what is pyonephrosis and presentation
pyelonephritis +hydronephrosis (infection of the kidney) Loin pain fever Nausea and vomiting haematuria proteinuria sterile pyuria leads to sepsis
treatment of pyonephrosis
Iv antibiotics (gentamicin) + oxygen + drain watch for sepsis and potentially transfer to ITU
what does Acute kidney injury mean
Spectrum of kidney disease ranging from mild improvement to full kidney failure requiring RRT
What is creatinine and why is it used in
its a muscle breakdown product that is filtered freely in the kidney and not reabsorbed so gives indication of kidney filtration levels. elevated serum creatinine suggest reduced filtration
criteria to diagnose AKI
> 26 mmol/L rise in serum creatinine
50% increase in serum creatinine
oliguria less than 0.5ml/kg/Hr
what is the time frame for acute kidney injury and chronic kidney injury
3 month
risk factors for kidney injury
Diabetes liver disease sepsis reduced fluid intake age >75 CKD Cardiovascular problems PMH of urinary symptoms urinary symptoms Drugs - NSAIDs and ACEi
why can NSAIDs and ACEi have an effect on Kidney
Prostaglandins cause afferent dilation which improves GFR
Angiotensin 2 causes efferent constriction whic also improves GFR
having ACEi and NSAIDS blocks this and causes Reduced GFR
causes of AKI
commonest are ischemia, sepsis, nephrotoxins
Pre renal - commonest cause (70%)
renal-
Post renal causes- least common
causes of AKI
pre renal
hypoperfusion, any reason. HV shock, D and V , sepsis
ACEi or NSAIDs.
renal artery stenosis
causes of AKI
renal
acute tubular necrosis (commonest renal cause of AKI)
glomerular cause, autoimmune, SLE, or Glomerulonephritis
interstitial, drugs like aminoglycans
vascular: SLE, ischemic, increased BP
causes of AKI
post renal
any obstruction to outflow tract-
lumina, stones, clots
intramural, BPH, Malignancy of bladder, ureter, prostate
extraluminal: compressive malignancy
What can cause Acute tubular nephrosis
nephrotoxins,
myoglobinuria by rhabdomyolysis
name some nephrotoxins
aminoglycans, Vancomycin
Lithium
Methotrexate
assessment and investigations of a patient with AKI
assess history: which drugs they are on, Risk factors PMH Urgent Hyperkalemia examination
Examination: look for palpable kidney (PCKD) bladder or masses in abdomen , check volume status- BP, JVP, edema, skin turgor.
bed tests: Dip stick, looking for nitrates or leukocytes, Microscopy and cultures to look for crystals, cultures
blood tests, U and E, FBC, clotting LFT, ESR, CRP, potentially serology
Imaging- renal USS, CTKUB,
Urgent examination to carry out in AKI
Urgent K+ and ECG checking for Hyperkalemia
Investigations and Imagining of AKI
Ultrasound looking for hydronephrosis or obstruction,
if hydronephrosis and over 65 suspect BPH and catheterise
if not relieved do NCCTKUB to look for stones etc
presentation of AKI
Usually asymptomatic and only detected on Blood tests but can present with nausea vomiting, confusion and a wide variety of symptoms (on another flashcard
Signs and symptoms of AKI
early: nausea, vomiting, reduced urine output, dizziness, lethargy
due to fluid retention, pul odema, nocturnal dyspnea, orthopnea, peripheral oedema
due to B, hyper or hypotension , Orthostatic hypotension, tachycardia
Confusion
haematuria
general managment of AKI
monitor for hyperkalemia assess fluid volume levels and aim to acheive euvolemia, give fluids or restrict fluids. stop any nephrotoxic drugs, stop NSAIDS, ACEi, Metfroim manage underlying dieseas
Managment of AKI
pre renal
renal
post renal
Pre renal, if spsis, antibiotics. fluid challange if not CCF
Post renal, catheterise, if that doesnt work then NCCT KUB to see if there was stone and clear
Renal- may need dialysis or refered to nephrologist
WHat are indications for dialysis in AKI
Fluid overload signs and symptoms, JVP, Oedema , Orthopnea, nocturnal Dysnpnoea
or Anuria
Hyperkalemia
metabolic acidosis
Uraemic complications like encephalopathy or pericarditis
drug overdose
Indications to refer AKI to nephrologist
Hyperkalemia
what are the complications of uremia
confusion coma
pericarditis pericardial rub
uremia induced platelet dysfunction, GI bleeds
neuropathy, nausea and vomiting, cramps
complications of AKI
Hyperkalemia
edema
uremia
acidosis
Prevention of AKI
monitoring drugs they are taking, temporarily stopping them if they have D and v
ensure patients in hospital are well hydrated use fluid volume charts
Med review if D and V
ECG changes of hyperkalemia
High T wave
absent P wave
increased PR interval
wide QRS
Treatment of Hyperkalemia
IV insulin and Glucose
since insulin stimulates uptake of Glucose
what is chronic kidney disease, time to become chronic
Renal impairment for more than 3 Months
how is chronic kidney disease staged and what symptoms are found at each stage
EGFR
stage 1 > 90 just has risk factors
stage 2 = 60-90 proteinuria
stage 3 = 30-59 still asymptomatic, N and V
stage 4 = 15-30 this is when symptoms usually start to show
end stage renal failure <15 - needs RRT at this stage
causes of CKD
Diabetes M type 2 more than 1 glomerulonephritis (commonest cause)- SLE, Vasculitis, nephropathy Congenital - PCKD Hypertension or renovascular disease Pyelonephritis following from AKI
Symptoms of CKD
symptoms usually start when there is uremia
Anaemia, Pallor lethargy SOB
Platelet abnormality - Bruising, epistaxis
Skin - pigmentation and pruritus and purpura
GI- anorexia, D and V nausea
Endo - amenorrhea, erectile dysfunction
CNS- confusion, encephalitis
CVD, Pericarditis, pericardial rub, hypertension cardiomegally
Renal- nocturia, polyuria
oedema and pul oedema, dyspnea orthopnea
MSK, weakness
commonest symptoms of CKD
Uraemic tinge, pigmentation
Increased BP
Fluid overload signs
Investigations and examination of CKD
look for signs of fluid overload and oedema- signs and symptoms, cardiomegaly
Bloods: HB, normal or normocytic anemia, ESR and CRP, Ca low , PTH high, PO4- low or High
Urinalysis: dipstick, Haematuria, (glomerulonephritis) proteinuria, suggests Glomerular disease. MSand C shows albumin creatinine conc
Biochem: creatinine clearance test, estimates GFR and is a screening tool
Renal ultrasound for all renal patients, look for hydronephrosis, do biopsy if still unknown
Management of CKD conservative
stop nephrotoxic drugs,
Limit progress, lower BP
Bone disease: use Vit D analouges to lower PTH
CVD: statins, Lifestyle and BP
Diet, avoid high phosphate food, Potassium restrictions
Management of CKD stage 1 to 4
Main cause of death is CVD
so ACEi or ARB plus statins plus diuretics plus CCB if needs be
Management of CKD symptoms
anemia, Iron B12 Folate
Acidosis, sodium carbonate
oedema, diuretics, loop diuretic furosemide
prepare for RRT
Treat underlying conditions, BPH, Diabetes
what is RRT and how to prep for it
Hemodialysis- insert AV fistula
Peritoneal dialysis
Renal transplant
what glomerular nephritis
disease of the glomerulus
term for inflammation of glomerulus and nephron
can have nephrotic or nephritic presentation
Nephrotic syndrome presentation
Proteinuria Mild hypertension Mild impairment of GFT Hypoalbuminemia Oedema
pathophysiology of nephrotic syndrome
Damage to podocytes so protein can leak though causing hypoalbuminemia and oedema .
due to reduced albumin in blood liver works more produced more albumin and causes Hyperlipidemia
causes of nephrotic syndrome
Primary, Membonous, minimal change, FSGS, focal segmental Glomerulosclerosis
Secondary- Diabetes, SLE Amyloid, Hep B or C
complication of Nephrotic syndrome
Due to loss of Immunoglobulins- increased risk of infection
due to hyperlipidemia, Increased Risk of Thromboemboli to Mi or Stroke
Treatment of Nephrotic syndrome
Oedema, Loop diuretic furosemide
Proteinuria: ACEi or ARB
Prevent atheromas by statins and anticoagulation
Treat underlying cause, usually steroids, glucocorticoids
Nephritic syndrome Presentation
Haematuria, Proteinuria, Oliguria
Mod to severe increase in BP and Decrease in GFR
nephritic syndrome Pathophysiology
Excess damage to nephron and glomerulus so Blood and protein leak though. reduction in GFR causes oliguria.
there is compensatory increase in BP
nephritic syndrome causes
Commonest cause is IgA nephropathy (primary cause)
other primary cause is mesangiocapillary GN
Secondary causes. SLE, ANti GBM disease, Goodpasture’s. Post streptococcus infection, Hep b or C
vasculitis
Drugs, penicillamine
Investigations for Glomerulonephritis
Bloods, FBC, U and E, LFT ESR CRP, Serology anti ANA, Anti DsDNA
Urinalysis - dip stick and MC and S- look for streptococcus, RBCs, WBCs, albumin
Renal Biopsy is gold standard-
management of Glomerulonephritis
Refer to nephrologist maintain Bp Diuretics for oedema (more in nephrotic) ACEi for proteinuria statins and anticoagulation diet for hyperlipidemia (more in nephrotic) Treat underlying cause potentially steroids or glucocorticoids Potential antibiotic therapy
nephrotic or nephritic syndromes that need Immunosuppressive therapy (prednisolone)
IgA nephropathy
SLE
Anti Glomerular basement membrane disease
Vasculitis
whos is screened for Chronic kidney disease
screen at risk patients Diabetes Hypertension CVD BPH Recurrent UTI Family history of ESRD Congenital kidney disease like PCKD
how is screening for Chronic kidney disease done
Albumin creatinine ratio
urinalysis
serum creatinine
What is polycystic kidney disease
inherited disorder either autosomal recessive or dominant.
Prevalence of PCKD and what gene does it affect
PKD1 and 2 on chromosome 16
1 in 1000
Progression of PCKD
85% progress to ESRD
can cause increased risk of forming renal stones and calculi
Signs for PCKD
Palpable kidney, Think PCKD Abdominal pain haematuria (from Cyst hemorrhage) Hypertension progressive renal failure SAH UTIs
pathophysiology of PCKD
cysts in kidney, causing enlargement. they can hemorrhage leads to haematuria
cyst infection can cause renal stones
Increased risk of renal cell carcinoma
extrarenal signs and pathology/complications of PCKD
liver cysts intracranial aneurysm- SAH ovarian cyst Diverticular disease Mitral valve prolapse
complications of PCKD
hypertension, increased cardiovascular morbidity and mortality, chronic renal failure, ruptured intracranial aneurysm, and end-stage renal disease
Investigations to confirm this is PCKD
Renal ultrasound
CT or MRI if not found on Ultrasound
Investigations to carry out in PCKD to assess damage and other complications
Urinalysis to look for UTI, increased albumin, haematuria. these indicate more likely to progress to severe disease
ECG - suspected LV dysfunction
Brain CT if suspected SAH
Can screen for SAH with MRI angiography
Management of PCKD
Monitor kidney function U and E
Control BP to 130/90
Treat Infections
if painful, Laparoscopic removal of cyst
Diet, increase water reduce sodium and avoid caffeine
ESRD, Dialysis or transplant
Screen relatives and genetic counseling
Screening for PCKD
Screen in relatives USS less than 40 YO, up to 3 cyst is normal 40-60 year old, Up to 2 cysts per kidney 60 or more up to 4 cysts per kidney
Who to screen for SAH
1st degree relative with PCKD plus SAH
Screen using MRI angiography
