Renal Flashcards
Definition of AKI?
What are the cut numbers for Cr, Urine & eGFR changes in AKI?
What’s the Cr & Urine changes in stage 1,2 & 3 AKI?
Definition:
Reduced kidney function resulting in oliguria, raised K, Cr & Urea, reduction in eGFR.
Creatinine:
-> or = 26mmol/L rise in Cr within 48hrs OR >=50% rise in Cr within 7 days.
Urine:
Oliguria is defined as urine output <0.5ml/kg/hr for 6 hours. So e.g weight is 60Kg then <30ml/hr urine output for 6hrs = oliguria.
-eGFR =>25% fall in 7 days.
Stage 1:
Cr inc. 1.5x baseline OR Urine output <0.5ml/kg/hr for 6-12hrs.
Stage 2:
Cr 2x & Urine Output <0.5ml/kg/hr >12hrs.
Stage 3:
Cr 3x & urine output <0.3ml/kg/hr for 24hrs.
Causes of AKI?
Prerenal:
- Hypovolemia from (vomiting/diarrheas, sepsis, cardiogenic shock)
- Renal artery stenosis
Intrinsic:
- Nephrotoxic drugs: ACE-i/ARB, NSAIDs, Aminoglycosides, diuretics, Contrast.
- Immune mediated glomerulonephritis
- Acute tubular necrosis
- Acute interstitial nephritis
- Rhabdomyolysis
- Tumor lysis syndrome
Postrenal:
- kidney or ureteric stones
- hydronephrosis & hydroureter
- extrinsic pressure from prostatic Ca, BPH
Who’s at increased risk of developing AKI (to be cautious when dealing with patients as 15% of hospital patients develop AKI)?
& how to prevent AKI?
1-Patients with failures (CKD,HF, LF, DM)
2-Previous AKI
3-On nephrotoxic drugs or have started it recently within 1 week including Contrast.
4-Age 65 & over
Prevention:
- IV fluids before & after contrast
- Stopping medications temporarily.
What happens when kidneys stop working (AKI)? i.e. signs & symptoms
1-Oliuria
2-Fluid overload (peripheral & pulmonary oedema)
3-inc. in molecules that should be flushed out (K, Cr, Ur) = arrhythmia & Uraemia (encephalopathy, pericarditis).
What Ix for AKI?
1-Urinalysis & Urea & Electrolytes.
2-USS of Kidneys within 24hrs (hydronephrosis/obstruction/urinary tract)
3-ECG for hyperkalaemic changes
4-CXR for pulmonary oedema & ABG for subsequent hypoxia.
A- Drugs safe to continue in AKI?
B-Should be stopped in AKI as might worsen the renal function?
C-May have to be stopped in AKI as inc. risk of toxicity but doesn’t worsen the AKI itself?
A-Paracetamol, Warfarin, Statins, Aspirin (75mg), Clopidogrel, Beta blockers
B-NSAIDS, Aminoglycosides, ACE-I, ARBs, Diuretics
C-Metformin, Lithium, Digoxin
Mx of AKI?
1-ABCDE
2-Pre-renal: fluids in hypovolemia, IV Abx if septic, STOP nephrotoxic drugs
Renal AKI: nephrology review
Post-Renal: Catheterize & review by urologists.
*treat any hyperkalaemia, pulmonary oedema, monitor regularly (obs, fluid status, urine output, U&Es).
Indication for dialysis in AKI?
AEIOU
Acidosis (severe metabolic acidosis with pH of <7.20)
Electrolytes imbalance (persistent hyperkalamia of >7mM)
Intoxication (poisoning)
Oedema (refractory pulmonary oedema)
Uraemia (encephalopathy or pericarditis)
CKD Definition?
What indicates chronic kidney disease? (kidney damage markers)
How would you confirm someone has CKD?
Gradual irreversible decline in kidney function due to fibrosed kidney parynchema (glomerulus, tubulues & interstitium, vasculature)
Kidney damage markers:
1-electrolyte abnormalities (high Ur, Cr & K) because the renal blood flow is reduced which leads to reduced filtration.
2-Reduced filtration rate means eGFR <60ml/min/1.73m2
3-Albuminuria (kidneys leak proteins out)
4-Structural & histological renal abnormalities
-Renal biopsy (helps find the underlying causes as well as confirm Dx)
What are the causes of CKD?
Most common: diabetic nephropathy, HTN, PKD, chronic glomerulonephritis (e.g. seconadry to SLE, or IgA nephropathy)
Others: Vascular (renal artery stenosis, Vasculitis), Myeloma, Amyloidosis, Congenital (Alport syndrome), developmental (vesico-ureteric reflux)
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Complications from CKD: Renal bone disease Pathophysiology & Mx?
1-Renal bone disease:
- Kidneys usually produce Vitamin D (so get Vitamin D deficiency)
- They normally excrete phosphate (so inc. in Phosphate levels)
- Vitamin D deficiency means Calcium isn’t absorbed from diet = low calcium levels
- The low Ca, Low Vitamin D & high Phosphate levels causes secondary hyperparathyroidism (high PTH).
Then the high PTH & phosphate cause resorption of Ca from bones leading to: reduced bone density (osteoporosis),
Low vitamin D=reduced bone mineralization (Osteomalacia)
Mx:
First line- control phosphate levels in diet
-Vitamin D: Alfacalcidol, calcitriol
-Phosphate binders: Either calcium based (give hypercalcemia & vascular calcification) or non-calcium based (Sevelamer).
Parathyroidectomy (optional)= if PTH>28mmol/L.
CKD: Other complications?
1-CVD: Tertiary hyperparathyroidism means high ca & Ph causing vascular calcification.
Explanation: after secondary hyperparathyroidism (from low vit D, low Ca & low Ph), the parathyroid gland works really hard to inc. Ca levels through bone resorption which works (blood levels of Ca inc.) BUT despite this achieved goal, the parathyroid gland goes into automation so keeps producing PTH (what we call tertiary hyperparathyroidism where the Calcium is high).
2-Inability excrete things:
A-Uremia (high BUN)= nausea, vomiting, anorexia, pericarditis, encephalopathy, pruritis, yellow ting.
B-Accumulation of organic acids= Metabolic acidosis with raised anion gap
C-Hyperkalemia = Arrhythmias
D-No fluid excretion= Fluid overload (Pulmonary oedema, Peripheral oedema, raised JVP)
3-Erythropoiesis production
5-Sensory neuropathy & leg restlessness
-How to detect diabetic nephropathy?
What happens if it develops?
What medications do patients need?
In diabetic nephropathy, microalbuminuria can happen. If it progresses, it can cause CKD & overt signs of nephropathy.
SO, all patients >12yrs old must undergo regular urinary albumin:creatinine ratio (ACR) to screen for microalbuminurea.
If its detected (>2.5mg/mmol in men & >3.5mg/mmol in women) = start ACE-inhibitor
How to Mx the sequelae of CKD?
Oedema= fluid & salt restriction. Furosemide (IV if acute).
Anaemia= monthly S/C erythropoietin (hb target 10-12g/dL). MUST resolve iron deficiency anaemia for it to work.
What types of renal replacement therapy?
- 1- DialysisHaemodialysisPeritoneal dialysis
- 2-Kidney transplant
PKD: What is it?
Differences between presentation in adults vs. infants?
Bilateral enlargement due to cysts in both medulla + cortex
- In Infants:Autosomal RecessiveLeads to: renal failure, HTN, portal vein HTN (hepatic fibrosis & hepatic cysts).
- In adults:Autosomal Dominant (APKD1 or APKD2)Leads to: HTN, Haematuria, CHF, Berry aneurysms, Hepatic cysts causing hepatomegaly, Mitral valve prolapse.
In adults can present as flank abdominal pain, early food satiety & hepatomegaly.
Renal colic: what is it?
Epidemiology of renal stones?
Pain that occurs due to a stone in urinary tract.
Peak Incidence
: 20-50 years old, 50% recurrence in 5-10yrs.
M:F
= 3:1 Women have higher urinary Citrate levels (protective factor), Men have testosterone which may increase Oxalate levels (risk factor)
Higher incidence
in caucasians & asians
Risk factors for renal stones & inhibitors of stones?
Risk Factors:
Diet-
Animal protein, salt, oxalate (in certain foods e.g. black tea, strawberries, green leafy veg, nuts, rhubarb)
Hot Climate
Infection
(Some bacteria produce Urease which makes urine more alkaline)
Abnormal anatomy/structure/foreign body
Poor mobility
- absorb Ca from bones (hypercalcaemia)
IBD/chronic diarrhoea
- affects oxalate levels due to Bile salt absorption
Chemotherapy, gout
(high uric acid),
hyperparathyroidism
(high Ca)
Supersaturation=> crystallization=>aggregation
Inhibitors of stones:
High fluid intake
Citrate
Types of stones & if radioopaque/lucent?
1-Calcium Oxalate (85%): Radiopaque
2-Struvite(20%): after infections
3-Uric acid (10%): Radiolucent
4-Calcium phosphate: radiopaque.
Renal Artery stenosis: how does it develop?
Epidemiology?
Features?
In young people: fibromuscular dysplasia
In older people: atherosclerosis
90% incidence in women
Features:
hypertension
chronic kidney disease or more acute renal failure e.g. secondary to ACE-inhibitor initiation
‘flash’ pulmonary oedema
What are the causes of haematuria?
1-Trauma:
Injury to renal tract
Renal trauma commonly due to blunt injury (others penetrating injuries)
Ureter trauma rare: iatrogenic via catheters
Bladder trauma: due to RTA or pelvic fractures
2-Infection: including TB
3-Malignancy:
Renal cell carcinoma (remember paraneoplastic syndromes): painful or painless
Urothelial malignancies: 90% are transitional cell carcinoma, can occur anywhere along the urinary tract. Painless haematuria.
Squamous cell carcinoma and adenocarcinoma: rare bladder tumours
Prostate cancer
Penile cancers: SCC
4-Renal disease:
Glomerulonephritis
5-Stones:
Microscopic haematuria common
6-Structural abnormalities: Benign prostatic hyperplasia (BPH) causes haematuria due to hypervascularity of the prostate gland
Cystic renal lesions e.g. polycystic kidney disease
Vascular malformations
Renal vein thrombosis due to renal cell carcinoma
7-Coagulopathy
8-Drugs: Cause tubular necrosis or interstitial nephritis: aminoglycosides, chemotherapy
Interstitial nephritis: penicillin, sulphonamides, and NSAIDs
Anticoagulants
9-Gynaecological:
Endometriosis: flank pain, dysuria, and haematuria that is cyclical
10-Iatrogenic:
Catheterisation
Radiotherapy; cystitis, severe haemorrhage, bladder necrosis
11-Benign: exercise
Signs of Nephrotic Syndrome?
Causes of Nephrotic Syndrome?
Proteinuria: >3.5g/day, microalbuminuria, oedema, hyperlipidaemia
Glomerular causes: 1-Membranous 2-Minimal change 3-Membranoproliferative 4-Focal segmental
Systemic causes:
DM, HTN, Amyloidosis, drugs
Signs of Nephritic syndrome? Causes?
Proteinuria:1-3g/day, Haematuria
Glomerular Causes:
1-IgA
2-Post-streptococcus GN
3-Goodpasture’s syndrome
Vascular causes:
HSP
Churg-strauss
Wegener’s
How does Post-Streptococcus GN present?
Findings?
Common features with IgA nephropathy?
PSGN: presents 7-14days after URTI (especially group A Beta-haemolytic strep infection for example streptococcus pyogenes)
Young children usually, present with headache, malaise, oliguria, visible haematuria, proteinuria/oedema, HTN.
Findings:
Blood: low C3, ASO is raised.
Renal biopsy: acute, diffuse proliferative glomerulonephritis & endothelial proliferation with neutrophils.
Electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
Immunofluorescence: granular or ‘starry sky’ appearance
Good prognosis!
Similarities with IgA: URTI & visible Haematuria
