Renal workbook Flashcards
How do you perform a renal examination

Renal Ix
- Bloods:
Hb (reduced EPO), WCC (pyelo)
U&E: K (elevated in CKD), urea, creatinine, bicarbonate (dec less absorption in CKD)
Bone profile (CKD dec vit D and Ca absorption) high PTH, high ALP due to damage/resorption?
Renal mets: bones, liver, lungs, brain, and distant lymph nodes
LB
Urine protein: creatinine ratio: a ratio of <0.2 is equivalent to 0.2 g of protein per day and is considered normal, a ratio of 3.5 is equivalent to 3.5 g of protein/day and is considered nephrotic-range (or heavy) proteinuria.
albumin (mcg/L) to creatinine (mg/L): <30 is normal; a ratio of 30-300 signifies microalbuminuria and >300 are considered as macroalbuminuria. On a standard urine dipstick, 10-20 mg/dL is the minimal detection limit of protein.

Metabolic acidosis causes
Metabolic acidosis is classified according to the anion gap. (Na+ + K+) - (Cl- + HCO-3). The normal range = Normal Anion gap is 8-12
Normal anion gap ( = hyperchloraemic metabolic acidosis)
- gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
- renal tubular acidosis
- drugs: e.g. acetazolamide
- ammonium chloride injection
- Addison’s disease
Raised anion gap
- lactate: shock, sepsis, hypoxia
- ketones: diabetic ketoacidosis, alcohol
- urate: renal failure
- acid poisoning: salicylates, methanol
Metabolic acidosis secondary to high lactate levels may be subdivided into two types:
- lactic acidosis type A: sepsis, shock, hypoxia, burns
- lactic acidosis type B: metformin

Causes of hypekalaemia, signs, treatment

Hypokalaemia causes, signs, treatment
reefeding syndrome spike in insulin

- Many patients with early AKI may experience no symptoms. However, as renal failure progresses the following may be seen:
- RF, stages, causes, and Ix for AKI

1.
- reduced urine output
- pulmonary and peripheral oedema
- arrhythmias (secondary to changes in potassium and acid-base balance)
- features of uraemia (for example, pericarditis or encephalopathy)
- image
cANCA is associated with?
pANCA is associated with?

- What drugs to stop in AKI
- Indications for RRT
- Acidosis
Electrolytes (hyperkalaemia)
Intoxications – ethylene glycol, methanol, salicylates, lithium
Overload (refractory to diuretics)
Uraemic pericarditis, Uraemic encephalopathy – vomiting, confusion, drowsiness, reduced consciousness

Glomerulonephritis
- Nephrotic definition: (podocyte damage)
- Complications of nephrotic syndrome:
- Causes of Nephrotic syndrome:
- Nephritic syndrome
Presentation can vary in a combination of some or many of the following:
1.
- Oedema
- Albumin <30
- Urine PCR >350 (proteinuria > 3.5g/24 hours)
- Hypercholesteraemia
2.
- Higher risk of Infection
- VTE
- Progression of CKD
- HTN
- Hyperlipidaemia
3.
- Minimal Change Disease – most common form of GN in children
- Focal Segmental Glomerulosclerosis – Idiopathic or secondary to infection, malignancy, drugs etc.
- Membranous Nephropathy – Idiopathic or secondary to infection, malignancy, drugs etc.
- Membranoproliferative Glomerulonephritis (more commonly presents as nephritic syndrome)
- Amyloidosis/Myeloma/Diabetes may have nephrotic range proteinuria but not necessarily other nephrotic features
4.
- AKI (sometimes GFR can drop drastically)
- On urine dipstick: blood +/- and/or protein+/- Mild to moderate oedema
- Proteinura <3.5g/24 hours
- HTN
- Sometimes visible haematuria

State the associations, Ix findings and Rx for
- Post-streptococcal GN (now called Post-infectious GN),
- IgA Nephropathy,
- Small vessel vasculitis (ANCA associated vasculitis),
- Anti-GBM Disease (Goodpasture Syndrome)
pulmonary haemorrhage (haemoptysis), can lead to RPGN.

- Thin Basement Membrane Disease, Alport Syndrome and Lupus Nephritis
- Management of Glomerulonephritis:
- Supportive therapy
- If suspect GN – discuss with Renal team
- MDT approach depending on underlying diagnosis
- ACEi/ARB for proteinuria
- Control BP
- Salt and water restriction if volume overloaded
- Diuretics for fluid overload
- If hypoalbuminaemic <20g/dl then higher risk for VTE – consider therapeutic LMWH
- Statins for hypercholesterolaemia
Immunosuppressive therapy:
- Specific to cause of GN – decided by Renal team (+/- Respiratory / Rheumatology teams if lung or systemic involvement )
- Oral Corticosteroids, IV pulsed methylprednisolone, Cyclophosphamide, Tacrolimus, Ciclosporin, Rituximab, MMF, Azathioprine
Invasive therapy
- Renal replacement therapy/haemodialysis for those in severe AKI or ESRF
- Plasma exchange for AAV, anti-GBM,
THIN FOUR MONITOR
ALPORT 5 LAND AND TAKE OF

Chronic Kidney Disease
- Definition
- classification
- causes
- complications
- Rx
eGFR <60 can get 20mg statins

- CKD is defined as the presence of kidney damage, manifested by abnormal albumin excretion or decreased kidney function, quantified by measured or estimated GFR that persists for more than three months.
Dyslipidaemia statins esp if diabetic
Diabetic Nephropathy
- how do you diagnose
- how do you treat
Hypertensive Nephropathy (nephrosclerosis)
- Investigations to identify if primary or secondary HTN (based on clinical findings and index of suspicion):
- Treatment
Polycystic Kidney Disease
- 2 Types (both are autosomal dominant):
- Symptoms?
- Diagnosis/Ix
- Treatment
- Many factors contribute to Anaemia in CKD, Management of Anaemia of CKD
- CKD- MBD can be diagnosed if a patient with CKD has evidence of one or more of:
- CKD leads to
- Raised Urine Albumin: Creatinine Ratio/PCR
Evidence of long-standing/poorly controlled DM
Evidence of other microvascular disease (reitnopathy, peripheral neuropathy)
2.
- dietary protein restriction
- tight glycaemic control
- BP control: aim for < 130/80 mmHg using ACE inhibitors (ACE-i)
- control dyslipidaemia e.g. Statins
- screens – eye checks and foot checks
3.
- 24 hour urinary metanephrines (Phaeochromocytoma)
- Aldosterone: Renin ratio (Primary aldosteronism)
- Cortisol & Dexamethasone suppression test (Cushing’s syndrome)
- TSH (hyperthyroidism)
- MRA (Renal artery stenosis)
- Anti-hypertensives (see ABCD guidelines)
- Type 1 (85%; PKD1 mutation on Chromosome 16)
Type 2 (15%; PKD2 mutation on Chromosome 4)
- depend on the size of the kidney, infection of the cysts (flank pain, haematuria, and fever) or can be asymptomatic
- Family history is KEY
USS
Ultrasound diagnostic criteria (in patients with positive family history):
- two cysts, unilateral or bilateral, if aged < 30 years
- two cysts in both kidneys if aged 30-59 years
- four cysts in both kidneys if aged > 60 years
8.
- Control BP
- As per CKD management
- Tolvaptan (Vasopression receptor-2 antagonist) is available for some patients to slow progression of CKD.
- Genetic counselling and testing

- Describe how vitamin D is activated
- Tertiary Hyperparathyroidism
- Management of CKD-MBD
- Alfacalcidol is Vitamin D-hormone analog which is activated by the enzyme 25-hydroxylase in the liver
2.
- Occurs when PTH release continues despite raised serum Calcium levels (independently)
- As a result of parathyroid gland nodular hyperplasia
- Consequence of advanced CKD
- (1) The occurrence and/or severity of renal bone disease
(2) Cardiovascular morbidity and mortality caused by elevated serum levels of PTH and high phosphate levels and calcium overload.

Renal Replacement Therapy
- Peritoneal Dialysis: what is it, adv, disadv, Complications
- What is automated PD, continuous ambulatory PD, Assisted Automated PD

- peritoneal membrane acting as the dialysis membrane
Adv: QoL, excellent first choice for patients starting dialysis, particularly when they still have some residual native renal function, regimes are designed on a much more indiv basis than patients on HD.
Dis: manage technical aspects of dialysis, Unsuitable in patients with stoma/previous surgery, peritonitis
Complications – drainage problems, malposition, leaks, herniae, hydrothorax, long term use associated with encapsulating peritoneal sclerosis
2.
- night, 10-12L usually exchanged, over 8-10 hours
- 4-5 dialysis exchanges per day (usually 2 litres each
- Trained healthcare assistants visit the patient’s home tohelp with setting up APD.

- How does dialysis work
- Adv and disadv
- Explain these types of HD: Home HD, Nocturnal HD, CRRT
- Transplantation adv and disadv
- when shall we initiate Active Conservative Management

- image
- Efficient, support at unit
- Infection/Bacteraemia
- Haemodynamic instability
- Reactions to dialysers
- Haematomas/risk of bleeding
- Muscle cramps
3.
Home HD – offer training at home for more frequent HD
Nocturnal HD – Overnight slow, long HD
CRRT – continuous renal replacement therapy mainly used in acute setting (ITU/HDU)
- Adv: Near normal lifestyle, Better mortality/morbidity
Disadv:
- Criteria to meet suitability to safely undergo operation
- Compliance with medication lifelong
- Risk of rejection
- Risk of malignancies over time
- Risk of infection (on immunosuppression)
- Long waiting times for cadaveric organ
5.
- Age >80 OR
- WHO performance score of 3 or more

Renal Transplantation
- Important to document immunisation episodes ? as immunised patients are more difficult to cross- match
- CI for kidney transplantation
- What are the three types of transplants
- Induction treatment:
- Maintenance treatment (used immediately after transplantation and for long term to prevent acute or chronic rejection):
- (blood transfusion, pregnancies, prior transplant)
- Active infection or malignancy
Severe heart disease not suitable for correction
Severe lung disease
Reversible renal disease
Uncontrolled substance abuse, psychiatric illness
On-going treatment non-adherence
Short life expectancy
- Living Related Donor Transplantation (best)
- elective procedure, from selected donor that might have a good compatibility
- Time to transplantation can happen in months
Living Unrelated Donor Transplantation
- 4 forms:
a) live-donor paired exchange
b) live-donor/ deceased-donor exchange
c) live-donor chain
d) altruistic donation - Usually have comparable outcomes to live-related donors
- Time to transplantation can happen in months
Deceased Donor Transplantation (~ 60%)
- Patients receive a kidney (or two from the same donor) with little time for preparation, so transplant protocols are important to keep updated regularly
- Time to transplantation happen in years
- Survival of kidney allograft and patients are significantly low compared to live donor transplantation.
- Methylprednisolone AND:
basiliximab and thymoglobulin
OR less commonly used are alentuzumab and rituximab.
5.
- Steroids: prednisolone (or prednisone)
- Calcineurin inhibitors (CNI): tacrolimus, cyclosporine, voclosporin
- Antimetabolite medications: mycophenolate, azathioprine
- Rapamycin inhibitors: sirolimus and everolimus
- T-cell regulation: Belatacept and belimumab

Long term care of the transplant pt:
- Firsts months, follow up happens several times a month, after 6 months it happens less often
- Monitor GFR, CNI levels, proteinuria, Ca, phosphate and PTH, lipids and glucose
• Screen for infections (common and opportunistic)
• Vaccination (except live or live attenuated viral vaccines)
- Monitor and control cardiovascular disease, bone and mineral metabolism disease
- Screen for malignancies as patients are three times more likely to have any cancer
- Annual skin checks for skin cancers
- Contraception is obligatory in the first year, counsel about pregnancy one year after
- Mortality is related to: cardiovascular disease, infections and malignancies

Complications of transplantation
Simultaneous kidney transplantation
Acute (<1month): surgery or infections
<4 weeks: nosocomial infections or related to donor
1-12 months: activation of latent infections, relapsed, residual or opportunistic infections, community
>12 months: community acquired
Important germs to consider:
CMV, hepatitis B, Herpes simplex virus, Varicella zoster, EBV, BK; Aspergilllus, Pneumocystis jirovecii, Listeria, Mycobacterium tuberculosis, Toxoplasma gondii
Within the first year, some patients can develop new-onset diabetes after transplant (NODAT); important to remember personal risk factors and new factors, such as medications and a new gluconeogenic kidney.
malignancies: skin, cervix, breast, prostate, renal and urothelial, liver, colorectal, and lymphoproliferative disease. This last one in particular is common in patients with EBV.
Liver-kidney: patients with liver failure or cirrhosis and ESRF can be candidates for simultaneous transplant
Pancreas-kidney: selected patients with Type 1 diabetes mellitus. Can be done simultaneous or sequential
Patients with kidney transplant who progress into ESRF can be re-transplanted

Loop, thiazides, K+ sparing, carbonic anhydrase, corticosteroids
State the below for each
Examples
Main Indications
Action
Metabolism
Excreted
Common Side Effects
Other important Info

Patients with nephrotic syndrome are at a higher risk of VTE due to the
loss of anti-thrombin III. Anti-thrombin III inhibits antagonises the action of thrombin and therefore loss of anti-thrombin results in unopposed thrombin activity creating a pro-coagulant state and therefore prophylactic LMWH is recommended.
Obesity, growth retardation and papilloedema are complications of corticosteroids, which are commonly used in the management of nephrotic syndrome.
Haemorrhagic cystitis is a common complication of cyclophosphamide, another drug used in the management of nephrotic syndrome. However, haemorrhagic cystitis is not a recognised complication of nephrotic syndrome.