CSI - Urinary Retention/Chronic Kidney Disease

Question 1

What is GFR? What does it stand for and what does it correlate with?

Answer 1

• GFR - glomerular filtration rate
• tells us what volume of fluid is filtered from the glomerular capillaries into the bowman’s capsule per unit time
• GFR correlates with kidney function - reduction in GFR means that the kidney has a reduced capacity/function

Question 2

What is GFR proportional to?

Answer 2

• proportional to the clearance rate of any substance that’s freely filtered and neither reabsorbed nor secreted by the kidneys
• you can use the pslama concentration, urine concentration and rate of urine production to calculate the clearance rate

Question 3

What can we use to measure GFR?

Answer 3

• Creatine - it is an endogenous substance that is freely filtered and NOT reabsorbed
• a little bit is secreted, but creatine is easy to estimate clearance as it is easy and doesn’t need to be injected into the patient

CLEARANCE OF CREATINE - ROUGHLY PROPORTIONAL TO GFR

Question 4

What is the formula for clearance?

Answer 4

clearance = urinary substance x urinary production rate/plasma (substance)

Question 5

Instead of using serum and urine concentratios of creatine and the rate of urine production to measure clearance, what can we use to estimate creatine clearance?

Answer 5

• use evidence base formula to estimate it. The estimates of creatine clearance can be used to estimate GFR based on serum creatine measurements
• most common is MDRD - Modification of Diet in Renal DIsease - this formula adjusts for age, ethnicity and gender

Question 6

What is the MDRD formula? Why would an 89 year old white female not have the same serum creatine as a young, black male? What does it also depend on?

Answer 6

• Modification of Diet in Renal Disease formula
• adjusts for age, ethnicity and gender
• creatine is generated from the conversion of creatine and creatine phosphate, most of which is found in the muscle
• serum levels of creatine are dependent on the filtration in the kidneys AND the total creatine amount produced
• If we didn’t adjust for these things, the formula could suggest a young healthy person had poor GFR and could wrongly indicate an elderly patient has a normal GFR
• creatine also depends on diet as some amino acids are precursors

Question 7

What is the gold standard test for GFR? Why would it be done?

Answer 7

• Isotonic method where radioactive tracer is injected into patient intravenously
• serum concentrations of tracer measured sequentially to measure clearance
• DONE IN RENAL CLINICS if creatine based estimations are not thought to be reliable

Question 8

What should albumin loss be roughly? Why is this?

Answer 8

• albumin is a medium size protein, roughly the same size as glomerular pores
• has a flexible ellipsoid dhape
• theoretically it can squeeze through a pore if present in the right orientation BUT THIS IS UNCOMMON - if it does happen, it should be fully absorbed and VERY LITTLE FILTERED - albumin loss should be less than 30 mg a day, usually less than 10mg

Question 9

Why is albumin a good prognostic marker for CDK - chronic kidney disease? What is macro and microalbuminuria?

Answer 9

• if the glomerulus is leaky, a larger amount of albumin gets filtered, this overwhelms the reabsorption capacity of tubules and gets lost in untine
• moderate albuminuria (microalbuminuria) is when there is albumin loss between 30-300mg a day. If it is moderate it for 3 months this is the diagnosis for CDK
  -Severe albuminuria (also called macroalbuminuria) refers to albumin loss of over 300 mg per day

Question 10

Why is albuminuria so important? What does this give more information about and why? What does it correlate with?

Answer 10

Not only can albuminuria predict progression of kidney disease, but it also gives us an idea as to
an individual’s more general vascular health. If they are losing protein in their kidneys because of
changes to the renal vasculature and to the glomerulus, chances are that similar processes are going on throughout the body. Albuminuria is therefore thought to be reflective of the integrity and health of systemic vascular endothelium. It has been found to correlate with cardiovascular risk outcomes and is a predictor of cardiovascular mortality in Type 1 and 2 diabetes

Question 11

What is the glomerulus? Why is it important? What molecules can pass through the filtration barrier?

Answer 11

The glomerulus in the kidney acts as a filter through which the proteins may or may not passaccording to their size and charge, and also the filtration pressure across the glomerulus. Low molecular weight proteins pass quite easily across the glomerular filtration barrier. Medium-sized
proteins have limited passage and large proteins shouldn’t ever cross it in healthy conditions

Question 12

What happens to proteins that pass through the glomerulus?

Answer 12

Proteins that pass through the glomerulus are now carried through the renal tubules, along with
the filtrate. Renal epithelial cells, particularly those in the proximal, convoluted tubule reabsorb
proteins from the filtrate, usually by a process of endocytosis. They take the protein up into the
cell and hydrolyse it into its constituent amino acids, which are then transported across the cells
basolateral membrane back into circulation.
Remember that this tubular reabsorption of protein is a saturatable process, but under normal
conditions, almost all filtered protein is reabsorbed

Question 13

What is the most abundant protein found in the urine and why?

Answer 13

Now a small number of proteins may either be secreted or shed from the kidney and urino-genital
tract and therefore end up in urine. For example, Tamm-Horsfall protein also known as Uromodulin
is secreted by the tubular epithelium even under normal conditions. It is thought to have antimicrobial properties. This Tamm-Horsfall protein is the most abundant protein found in normal
urine, and it all comes from secretion

Question 14

How much of the protein is lost in urine over 24 hours in a healthy person?

Answer 14

In a healthy person, less than 150 mg of proteins is lost in the urine over a period of 24 hours

Question 15

What is diabetic nephropathy?

Answer 15

Diabetic nephropathy is defined by albuminuria
(increased urinary albumin excretion
>3.4mg/mmol) and a progressive decline in the
glomerular filtration rate, during the long duration
of diabetes.

Question 16

What are the clinical features of diabetic nephropathy?

Answer 16

Clinical features
• Hypertension
• Oedema
• Retinopathy
• Neuropathy (Numbness and pain in the
lower extremities)
• Foot changes- Foot ulcers
• Haematuria
• Shortness of breath
• Nausea and vomiting

Question 17

What is the treatment and clinical management of diabetic nephropathy?

Answer 17

Treatment and Clinical Management
• Optimised diabetes control
• Optimised treatment of hypertension
• Reduced proteinuria using ARB or ACEi
• Smoking cessation
• SGTL2 inhibitor
• Renal transplant
• Dialysis

Question 18

How do you reduce the risks of kidney disease?

Answer 18

Reducing the risks of kidney disease
1. Maintain blood glucose within target range
2. Minimise blood pressure
3. Smoking cessation
4. Ensure well-balanced healthy diet and keep active.
5. Attend medical appointments → Early diagnosis of chronic kidney disease and monitor progression

Question 19

How does diabetic mellitus lead to diabetic nephropathy?

Answer 19

Pathophysiology
Diabetes mellitus is characterised by
hyperglycaemia and increased glomerular
pressure which promote glomerular mesangial
expansion and an ultimate fibrosis of the
glomerular basement membrane- mediated by
advanced glycation end products and TGF-beta.
Activation of renin-angiotensin system leads to
elevated angiotensin-II in diabetes mellitus,
ultimately inducing efferent arteriole
constriction.
→ Initial glomerular hyperfiltration
→ Sheer stress to glomeruli (pressure induced
damage) causes podocyte injury
→ Glomerular basement membrane permeability
to proteins (albumin)
→ Albuminuria

Question 20

What two clinical investigations are conducted within the annual diabetes review? What do they test for?

Answer 20

Diagnosis and Treatment
Two clinical investigations are conducted as part of the annual review:
1) Urine test (ACR)
2) Blood test (eGFR)
ACR: A sample urine test referred to as the albumin: creatinine ratio (ACR), this diagnostic test measures the proportion of excreted urinary albumin to creatinine. In patients with kidney disease, there is an elevated amount of albumin excreted, as detected by a raised ACR – signs of proteinuria.
eGFR: The estimated glomerular filtration rate is a first-line investigation for patients suspected with diabetic kidney disease, determining the level of renal function and respective stage of kidney disease. It uses creatinine level and standardises with other parameters including age, sex and ethnicity

Question 21

What is the treatment offered to someone who is at risk/suspected of diabetic kidney disease?

Answer 21

• Antihypertensives: ACE inhibitors, NSAIDs and angiotensin receptor blockers (ARBs).

N.B: ACE inhibitors and ARBs provide a protective function to glomerular filtration by reducing hypertension.
• Lifestyle advice: Support from a registered dietician. In patients with diagnosed diabetes, optimising
glycaemic control is essential.
• Late-stage kidney failure: Consider dialysis or kidney transplant

Question 22

What is the treatment offered to someone who is at risk/suspected of diabetic kidney disease?

Answer 22

• Antihypertensives: ACE inhibitors, NSAIDs and angiotensin receptor blockers (ARBs).

N.B: ACE inhibitors and ARBs provide a protective function to glomerular filtration by reducing hypertension.
• Lifestyle advice: Support from a registered dietician. In patients with diagnosed diabetes, optimising
glycaemic control is essential.
• Late-stage kidney failure: Consider dialysis or kidney transplant

Question 23

Briefy summarise the Renin-angiotensin system.

Answer 23

The liver secretes
angiotensinogen that is
proteolytically cleaved by
renin (an enzyme released
by juxta-glomerular cells)
into angiotensin-I.
Angiotensin converting
enzyme (ACE) converts
angiotensin-I to
angiotensin-II. AngiotensinII is a potential
vasoconstrictor, increasing
systemic blood pressure
and increases sympathetic
activity.

Question 24

What is the role of angiotensin-II in the RAS system?

Answer 24

Angiotensin-II
• Promotes sensation
of thirst
• Promotes ADH
secretion from
posterior pituitary
gland.
• Promotes aldosterone synthesis from the zona glomerulosa of the adrenal cortex
• Increased sodium reabsorption.
• Activation of sympathetic nervous system – release of noradrenaline to increase cardiac output.

Question 25

What does aldosterone do as a result of the RAS?

Answer 25

Aldosterone acts on tubule cells of the distal convoluted tubule, potentiating potassium secretion and sodium
reabsorption.
• Sodium reabsorption facilitates increased water retention.

Question 26

What are factors affecting RAS?

Answer 26

Factors affecting RAS
A reduction in renal perfusion pressure or a decrease in sodium load is detected by the macula densa, which
communicates with the juxtaglomerular cells lining the renal afferent arteriole.
• In response to low renal perfusion pressure → Renin is released by JG cells (Increased sympathetic
activity stimulating beta-1 receptors).

Question 27

What is the effect of angiotensin-II on the renal afferent arteriole?

Answer 27

Renal afferent arteriole Vasoconstriction Voltage-gated calcium channels open
and allow an influx of calcium ions

Question 28

What is the effect of angiotensin-II on the efferent arteriole?

Answer 28

Vasoconstriction (greater than the
afferent arteriole)
Activation of AT-1 receptor within the
endothelium of efferent arteriole

Question 29

What is the effect of angiotensin-II on mesangial cells?

Answer 29

Constriction leading to a decreased
filtration area
Activation of Gq receptors and opening
of voltage-gated calcium channels.

Question 30

What is the effect of angiotensin-II on the proximal convoluted tubule?

Answer 30

Increased sodium reabsorption Increased sodium/hydrogen ion
antiporter activity and adjustment of the
Starling forces in peritubular capillaries
to increase paracellular reabsorption

Question 31

What is aldosterone and what does it respond to?

Answer 31

Aldosterone
Aldosterone is a steroid hormone synthesised within the zona glomerulosa of the adrenal cortex, in response to
aldosterone synthase activity potentiated by the stimulation of angiotensin-II.
• Response to a decrease in blood pressure (via baroreceptors).

Question 32

What is the function of aldosterone?

Answer 32

Aldosterone Function
• Increased sodium reabsorption (Control’s reabsorption
of 35g Na/day)
• Increased potassium secretion (A consequence of
sodium reabsorption).
The change in voltage promotes an indirect stimulation of
proton secretion, there are additional direct effects of
aldosterone on the secretion of proton via alterations in the
expression of anion exchanges as H+-ATPase.
• Increased hydrogen ion secretion

Question 33

What happens if there is an EXCESS of aldosterone?

Answer 33

Aldosterone excess → Hypokalaemic alkalosis.
N.B: Acts on the distal convoluted tubule and cortical collecting
duct.

Question 34

What is the role of aldosterone in the cortical collecting duct?

Answer 34

Aldosterone in the cortical collecting duct
Aldosterone increases the transcription and ultimate synthesis of ENaC (Epithelial sodium channel), the
sodium potassium ATPase and sets of regulatory proteins.
• Coordinates increase in the number of sodium transporters, and their activity thereby increasing
sodium reabsorption

Question 35

What are ACE inhibitors?

Answer 35

ACE Inhibitors
ACE-inhibitors reduce angiotensin-II synthesis by inhibiting the conversion of angiotensin-I to angiotensin-II.
Net effect = Lowering blood pressure.
Examples: Ramipril, lisinopril and enalapril.
• Vascular effects: Vasodilation - increasing the vascular volume to accommodate and reduce blood
pressure.
• Diuretic effects → Reduces sodium uptake in the PCT
• Reduced aldosterone → Reduced sodium reabsorption within the distal nephron and will reduce the
osmotic difference between the tubular fluid and interstitium → Reduces water reabsorption. (Note
potassium secretion is reduced

N.B: There is an increase in tubular fluid osmolarity in the distal nephron.
Considering angiotensin-II is responsible for vasoconstriction of the efferent arteriole, the subsequent inhibition
of this effect will result in dilation, ultimately decreasing GFR

Question 36

What are the side-effects of ACE inhibitors?

Answer 36

Side-effects
• Dry cough (ACE-mediated conversion to inactive bradykinin metabolites is inhibited).
• Hyperkalaemia
• Headache
• Dizziness
• Fatigue
• Renal impairment
• Angioedema (rare)
ACE inhibitors are contraindicated in bilateral renal artery stenosis. The effect of angiotensin-II helps to maintain
GFR when renal perfusion is low (stenosis, volume depletion & elderly patients with CHF).
• Inhibiting Ang-II with ACEi and ARBs will result in acute kidney injury (AKI)

Question 37

What are the (3) most suitable drugs to treat diabetic nephropathy and why?

Answer 37

Ramipril – First line treatment, capacity to reduce CKD proteinuria, reduces glomerular pressure and glomerular
injury.
Insulin – Target’s hyperglycaemia
Atorvastatin- Target’s dyslipidaemia (High blood cholesterol causes sclerotic glomeruli)

Question 38

Structure of glomerulus: what is the adaptations of the glomerular capillary endothelium?

Answer 38

Endothelial Cells
The glomerular capillary endothelium
consists of fenestrae, with a diameter
corresponding to 70nm. These pores do
not restrict the movement of water and
proteins, however, provide a limit of
filtration to erythrocytes.

Question 39

Structure of the glomerulus: what surrounds the luminal surface of endothelial cells and why?

Answer 39

Surrounding the luminal surface of the
endothelial cells is glycocalyx,
consisting of negatively charged
glycosaminoglycans which hinder the
diffusion of negatively charged
molecules.

Question 40

What makes up the glomerular basement membrane and why?

Answer 40

Glomerular basement membrane
The basement membrane comprises
predominantly of type IV collagen,
heparan sulphate proteoglycans and
lamina.
• Heparin sulphate proteoglycans
→ Function to restrict the
movement of negatively charged
molecules across the basement
membrane.
1) Inner thin layer (Lamina rara
interna)
2) Thick layer (Lamina densa)
3) Outer dense layer (lamina rara
externa)
N.B: These layers help to limit the filtration of intermediate to large sized solutes.

Question 41

What are podocytes and what do they form?

Answer 41

Podocytes
Podocytes are specialised epithelial cells of the Bowman’s capsule, forming the visceral layer of the capsule. Footlike processes project from the podocytes and interdigitate to form filtration slits.
• Filtration slits are bridges formed by the slit diaphragm
(contains pores preventing platelets and plasma proteins
from filtering through the tubule).
• Negatively charged glycoproteins cover the podocytes →
Restricting filtration of large anions.
A filtration membrane is formed, composing of endothelial cells of the glomerular capillaries, the glomerular basement membrane and podocytes

Question 42

What is proteinuria?

Answer 42

Proteinuria is defined as the presence of additional proteins within the urine, typically accompanied with
elevated serum creatinine, an indication of renal dysfunction.

Question 43

What are nephrotoxic drugs?

Answer 43

Nephrotoxic drugs:
1) NSAIDs
2) ACE inhibitors
3) Aminoglycosides (Gentamicin)
4) Contrast agents (Contrast CT Scan)

Question 44

What is haemoglobinuria?

Answer 44

Haemoglobinuria
A condition in which haemoglobin is found in abnormally high concentrations in the urine, as a result of overflow.
• Haematuria: The presence of blood in the urine (Bleeding from the urinary tract, with intact
erythrocytes).

Question 45

What is overflow of proteins in the glomerulus? Give examples of what conditions cause this. What does this lead to?

Answer 45

Overflow:
Rhabdomyolysis- Low molecular weight proteins pass through the filtration barrier into filtrate within the
Bowman’s capsule. Myoglobinuria is the presence of myoglobin in the urine, myoglobin interacts with TammHorsfall protein in the nephron to form solid aggregates that obstruct the flow of fluid.
• Overflow proteinuria is associated with the rapid degradation of skeletal muscle (trauma, exercise,
specific toxins) – resulting in a release of muscle constituents into circulation, including myoglobin.
• Overflow of haemoglobin is due to intravascular haemolysis.
N.B: Tam-Horsfall protein (uromodulin) – Secreted by tubular epithelium.
An excessive amount of soluble plasma proteins passes through the fenestrae into the filtrate, despite a large
proportion of proteins being actively reabsorbed, the re-uptake proteins subsequently become saturated, and
their reabsorption capacity is exceeded – leading to excess protein being excreted into the urine.

Question 46

What is Tubular (Acute tubulointerstitial nephritis?

Answer 46

Tubular (Acute tubulointerstitial nephritis)
A frequent cause of AKI and is characterised as an immune-mediated infiltration of the kidney interstitium by inflammatory cells – resulting in the tubular dysfunction

• The capacity of carrier proteins to selectively reabsorb the proteins from the filtrate is impaired, leading
to an increased demand on functional units

Question 47

What does the degree of albumin loss indicate about the grading and classification of CKD?

Answer 47

Attending regular screening tests may support early diagnosis, and the degree of albumin loss contributes to the grading and classification of CKD.
• Albuminuria reflects the integrity and health of vascular epithelium, correlator for CVD outcomes and
mortality in type 1 and 2 diabetes

Question 48

What is the normal range of GFR for males and females?

Answer 48

Normal Ranges
Male: 90-140mL/min
Female: 80-125mL/min

Question 49

What is GFR proportional to?

Answer 49

GFR is proportional to the clearance of any substance that is:
1) Freely filtered
2) Not reabsorbed
3) Not secreted

Question 50

What is meant by GFR? How do you calculate it?

Answer 50

GFR: The volume of fluid filtered from the glomeruli into the Bowman’s capsule per unit time (mL/min).
• Sum of filtration rate of all functioning nephrons
GFR = Puf x Kf
Kf- Ultrafiltration coefficient (Product of membrane permeability and surface area available for filtration).
Changes in Kf will result in GFR imbalances

Question 51

What does a reduction in GFR lead to?

Answer 51

A reduction in GFR is a characteristic feature of renal disease – Accumulation of excretory products within
circulation.
• Elevation of serum creatinine is an indicator of poor filtration

Question 52

Why might the MDRD formula be inaccurate?

Answer 52

Unreliable Formula:
• Pregnancy: Plasma creatinine can lag behind
change. Filtrate rate increases and occurs
spontaneously, and thus a drop in serum creatinine.
May not be seen.
• End stage renal failure prior to dialysis: Creatinine calculations are overestimated, GFR decreases –
proportion of secreted creatinine to filtered increases (Low true GFR, creatinine clearance is not a
reliable parameter for stage 4/5 CKD).
• Acute kidney injury patients: Rate of increase in serum creatinine does not parallel the fall in GFR (Real
time GFR and creatinine values before and after an episode of AKI).
• Factors: Trauma (muscle atrophy), trimethoprim (inhibits tubular secretion), malnutrition (reduced), or
sepsis (reduced production of creatinine).
Caution: MDRD formula may be unreliable in patients who are at an extreme weight; are taking creatinine
supplements; are malnourished; have a muscle wasting disease; and are bodybuilders

Question 53

How do you diagnose CKD using albumin/creatine ratio of urine sample?

Answer 53

Adjustment of concentration
differences, estimation of proteinuria.
• Provides reasonable estimate
of protein loss.
• Used in diabetes- greater sensitivity

Question 54

How can you diagnose CKD using a urine dipstick?

Answer 54

Specific detection to albumin in urine. Unable to detect cases of proteinuria
due to poor sensitivity to myoglobin.
• False negatives

Question 55

How do you diagnose CKD using a 24 hr urine test?

Answer 55

Total protein collection in urine over
the course of 24 hours.
• Total protein <150mg.
• Normal albumin <30mg (5-
10mg)
• Majority of protein is uromodulin.
Impractical and inaccurate method.

Question 56

How can you diagnose CKD using random albumin concentration?

Answer 56

Random albumin concentration Detects the amount of albumin in the urine.
Unreliable method – depends on urinary concentration and patients individual hydration

Question 57

What are consequences of CKD?

Answer 57

-decreased excretion - hyperrtension, peripheral odema, weakness and fatigue, metabolic acidosis, gout, hyperparathyroidism
- decreased biosynthesis - anaemia, HPT
- altered metabolism - atherogenesis

Question 58

What is renal dysfunction?

Answer 58

Renal dysfunction
• Accumulation of metabolic waste substances within
circulation. Disrupted filtration mechanism will
subsequently lead to haematuria and proteinuria. (Low
serum protein, albumin deficiency).
• Hypertension (Water retention)
• Metabolic acidosis (Disrupted acid-base balance)
• Anaemia (Deficit in EPO production)
• Vitamin-D deficiency and secondary
hyperparathyroidism.
Low serum calcium concentrations and serum calcitriol reduces negative feedback effect, parathyroid hormone secretion from chief cells accommodate hypocalcaemia

Question 59

Why does hyperparathyroidism occur in CKD?

Answer 59

Renal dysfunction is attributed to an impairment in the activity of renal 1-alpha-hydroxylase activity, therefore
the second hydroxylation of 25-cholecalciferol to active Vitamin-D is reduced.
• Hypocalcaemic conditions arise.
• Low serum calcium concentrations are detected by calcium-sensing G coupled chief cells in the
parathyroid glands – stimulates PTH synthesis and release.
PTH stimulates osteoclastogenesis, binding to PTH receptors potentiating the release of OAF & RANKL, and the activation of osteoclasts to resorb bone (releasing calcium ions from calcium hydroxyapatite).
PTH causes phosphate excretion from the distal convoluted tubule. In CKD, phosphate excretion is impaired, resulting in an elevation in serum phosphate.

Question 60

How does CKD affect FGF-23, NPT2 and calcitriol?

Answer 60

FGF-23 concentrations are elevated and is secreted by osteocytes.
• Decreases expression of NPT2 and suppresses calcitriol production.

Question 61

How does CKD progress with type 2 diabetes?

Answer 61

CKD progression in type 2 diabetes
• Moderate and normal albuminuria do not express a significant difference with their trends of renal
decline.
• Severe albuminuria exhibits a faster decline in renal function.
• There is a noticeable improvement in eGFR within the first 2 years – initiation of drug treatment for CKD.

N.B: Drug treatment does not prevent the inevitable progression of CKD

Question 62

How can you slow rates of GFR decline?

Answer 62

Multifactorial interventions slow rates of GFR decline to improve morbidity and mortality of patients with CKD.
Early recognition is required to minimise progression of renal disease, which is supported by adequate screening.

Question 63

How do you treat volume-overload in CKD?

Answer 63

Volume overload:
• Sodium and intravascular volume balance are usually maintained via homeostatic mechanisms until
eGFR <10-15mL/min/1.73m2.
Treatment: Sodium restriction and diuretic therapy (loop diuretics – furosemide)

Question 64

How do you treat hyperkalaemia in CKD?

Answer 64

Hyperkalaemia:
• Develops in patients who become oliguric (less urine reaches distal tubule), those with high potassium
diet, increased tissue breakdown or hypoaldosteronism.
N.B: ACE inhibitors and mineralocorticoid antagonists (spironolactone) increases the risk of hyperkalaemia.
Treatment: Low potassium diet and avoid using drugs that raise serum potassium.

Question 65

How do you treat metabolic acidosis in CKD?

Answer 65

Metabolic acidosis:
• Increasing tendency to retain hydrogen ions with progressive CKD.
Treatment: Bicarbonate supplementation, requires careful monitoring of volume status since bicarbonate is
administered with sodium, which can promote water retention.

Question 66

How do you treat mineral and bone disorders in CKD?

Answer 66

Mineral and Bone disorders
Causes renal osteodystrophy – changes in bone structure are an almost universal finding with progressive CKD.
• Osteitis fibrosa, osteomalacia, and adynamic bone disease. Osteitis fibrosa results from secondary
hyperparathyroidism and features weakened bone, where the calcified mineral elements have been
resorbed and replaced with fibrous tissue.
Treatment: PTH levels are earliest markers for abnormal mineral and bone metabolism in CKD.
• Dietary phosphate restriction, the administration of oral phosphate binders (reduce absorption of
dietary phosphate).
• Administer calcitriol – Suppress PTH secretion
• Vitamin D replacement – Circulating calcitriol levels decline when eGFR <40, markedly reduced in
patients with ESRD, phosphate retention reduces calcitriol production, therefore replacement therapy
addresses these complications.

Question 67

How do you treat sexual dysfunction in CKD?

Answer 67

Sexual dysfunction
• >50% of men with uraemia complain of symptoms that include erectile dysfunction, decreased libido
and decreased frequency of intercourse.
Females: Disturbance in menstruation and fertility – amenorrhea.
N.B: Plasma creatinine >265micromol/L in pregnant female uncommon

Question 68

How do you treat dyslipidaemia in CKD?

Answer 68

Dyslipidaemia
• Statin to correct LDL.

Question 69

How can you monitor and treat anemia in CKD?

Answer 69

Anaemia
Normochromic and normocytic anaemia
due to reduced production of erythropoietin
and shortened RBC survival.
• Anaemia is a common feature in
patients with CKD.
Monitoring
• Haemoglobin concentration monitored every 3-12 months (depending on stage of CKD) – begin anaemia
investigations in CKD patients when Hb level is <120Mmg/dL in females, and <130mg/dL in males.
Diagnosis:
• Include red blood cells indices, reticulocyte count, serum iron, total iron binding capacity, transferring
saturation, serum ferritin, B12 and folate concentrations and testing for blood in stool.

Treatment: Recombinant EPO drugs used to correct the anaemia

Question 70

How can you treat hypertension in CKD?

Answer 70

Hypertension
Combined therapy or diuretic and ACEI/ARB to reduce progression of CKD and
cardiovascular complications.
• Loop diuretic for oedema +
hypertension.
• Thiazide diuretics become less
effective as monotherapy (GFR
<20), reduced distal volume
renders ineffective,
• Arteriole pressure >100mgHg
Target in patients with diabetes:
130/80mmHg

Question 71

How can you treat hypertension in CKD?

Answer 71

Hypertension
Combined therapy or diuretic and ACEI/ARB to reduce progression of CKD and
cardiovascular complications.
• Loop diuretic for oedema +
hypertension.
• Thiazide diuretics become less
effective as monotherapy (GFR
<20), reduced distal volume
renders ineffective,
• Arteriole pressure >100mgHg
Target in patients with diabetes:
130/80mmHg