disorders of renal funct ion

BYD R K D D E L E - I J A G B U L U ( M B C H B )

D E P T O F FA M I LY M E D I C I N E

outline

• anatomy and physiology

• disorders of the renal system

• acute kidney injury

• chronic kidney disease

• glomerular disease

• nephrolithiasis

• polyuria

• renal acidosis

• hiv-associated nephropathy

the kidney: a n a t o m y a n d p h y s i o l o g y

anatomy of the kidneys

• The kidneys are paired bean-shaped retroperitoneal structures

located between the transverse processes of T12-L3 vertebrae

• The left kidney is located slightly more superior in position than the

right because of the liver on the right.

• The kidney is made up of three main parts: the outer cortex, the

medulla and the renal pelvis.

anatomy of the kidneys…

• The Nephrons which are the urine producing functional

structures in the kidney span the cortex and the medulla

(mainly medulla)

• The renal pelvis collects the urine; then urine is transported

out of the kidneys through the ureters into the bladder.

• Neurovascular supply: Renal artery and Renal Plexus

the nephron

Histologically,

The functional renal unit is the nephron.

It composed of the following:

– The renal corpuscle: Glomerulus and Bowman capsule

– Proximal convoluted tubules (PCT, located in the renal cortex)

– Descending loop of Henle (LOH)

– Ascending limb (which resides in the renal medulla)

– Thick ascending limb

– Distal convoluted tubule

– Collecting duct (which opens into the renal papilla)

the nephron

the renal corpuscle • This consists of glomerulus and bowman capsule

functions of the kidneys• Filtration and excretion of metabolic waste products and toxins (urea &

ammonium)

• Regulation of electrolytes, fluid, and acid-base balance

• Stimulation of red blood cell production

• Regulation of blood pressure via the renin-angiotensin-aldosterone system,

controlling reabsorption of water and maintaining intravascular volume

• Reabsorb glucose and amino acids

• Hormonal functions via erythropoietin, calcitriol, and vitamin D activation

functions of the kidneys…

d i so rde r s of the rena l s y s tem

disorders of the renal system

They include the following conditions:

• Acute Renal Failure (ARF)

• Chronic Renal Failure (CRF)

• Glomerular disease

• Nephrotic syndrome

• Nephritic Syndrome

• Polyuria

• Renal stones (Nephrolithiasis)

• Renal acidosis

• HIVAN

acute kidney in jur y

acute kidney injury

• Acute Kidney Injury (AKI), (previously Acute Renal Failure ARF), is defined as an abrupt decline in the renal filtration function.

• This deterioration in glomerular filtration rate (GFR) occurs over hours to 7 days.

• Retention of nitrogenous waste products, oliguria (urine output <400 mL/d), and electrolyte and acid-base abnormalities are frequent clinical features

• ARF is usually asymptomatic and diagnosed when biochemical monitoring of hospitalised patients reveals a new increase in blood urea and serum creatinine concentrations.

acute kidney injury: causes

Three major categories:

• Prerenal ARF: diseases that cause renal hypoperfusion, resulting in

decreased function without frank parenchymal damage

• Intrinsic ARF: diseases that directly involve the renal parenchyma

• Post-renal ARF: diseases associated with urinary tract obstruction

acute kidney injury: causes…

pre-renal causes…

acute kidney injury: pre-renal causes…Hypovolemia

• Increased extracellular fluid losses:

– haemorrhage

• Gastrointestinal fluid loss:

– vomiting, diarrhoea, enterocutaneous fistula

• Renal fluid loss:

– diuretics, osmotic diuresis, hypoadrenalism

• Extravascular sequestration:

– burns, pancreatitis, severe hypoalbuminemia (hypoproteinaemia)

• Decreased intake:

– dehydration, altered mental status

acute kidney injury: pre-renal causes…Altered renal haemodynamic resulting in hypoperfusion

• Low cardiac output state:

– diseases of the myocardium, valves, and pericardium (including tamponade); pulmonary hypertension or massive pulmonary embolism; impaired venous return

• Systemic vasodilation:

– sepsis, antihypertensives, afterload reducers, anaphylaxis

• Renal vasoconstriction:

– hyperCalcemia, catecholamines, calcineurin inhibitors, amphothericin B

• Impairment of renal auto-regulatory responses:

– cyclooxygenase inhibitors (NSAIDS), angiotensin-converting enzyme inhibitors, or angiotensin II receptor blockers

• Hepato-renal syndrome

clinical assessment: pre-renal arf

Symptoms:

• thirst and orthostatic dizziness

Physical signs:

• orthostatic hypotension, tachycardia, reduced jugular venous pressure,

decreased skin turgor and dry mucous membranes

Others include:

• stigmata of chronic liver disease and portal hypertension, advanced

cardiac failure, sepsis, or other causes of reduced "effective" arterial

blood volume

intrinsic renal causes…

intrinsic arf

1. Renovascular obstruction

2. Diseases of the glomeruli or vasculature

3. Acute tubular necrosis

4. Interstitial nephritis

5. Intratubular obstruction

acute kidney injury: intrinsic renal causes…1. Reno-vascular obstruction

• This may be bilateral or unilateral (in the setting of one kidney). Examples:

• Renal artery obstruction:

– atherosclerotic plaque, thrombosis, embolism, dissection aneurysm, large vessel vasculitis

• Renal vein obstruction:

– thrombosis or compression

acute kidney injury: intrinsic renal causes…2. Diseases of the glomeruli or vasculature

• Glomerulonephritis or vasculitis

• Others: thrombotic micro-angiopathy, malignant hypertension, collagen

vascular diseases (SLE, scleroderma), DIC, PET

acute kidney injury: intrinsic renal causes…3. Acute tubular necrosis

• Ischemia:

– causes same as for prerenal ARF, but generally the insult is more

severe and/or more prolonged

• Infection

– with or without sepsis syndrome

• Toxins:

– Exogenous (radiocontrast, antibiotics ,chemotherapy)

– Endogenous (rhabdomyolysis, haemolysis )

acute kidney injury: intrinsic renal causes…4. Interstitial nephritis

• Allergic:

– antibiotics (-lactams, sulfonamides, quinolones, rifampin), NSAIDS,

diuretics, other drugs

• Infection:

– pyelonephritis (if bilateral)

• Infiltration:

– lymphoma, leukemia, sarcoidosis

• Inflammatory:

– Sjögren's syndrome, tubulointerstitial nephritis with uveitis

acute kidney injury: intrinsic renal causes…5. Intratubular obstruction

• Endogenous:

– myeloma proteins, uric acid (tumor lysis syndrome), systemic oxalalosis

• Exogenous:

– acyclovir, gancyclovir, methotrexate, indinavir

clinical assessment: intrinsic renal disease

Diseases of small vessels and glomeruli

• Glomerulonephritis/vasculitis :

– New cardiac murmur (post-infectious)

– Skin rash/ulcers, arthralgias (lupus)

– Sinusitis (anti-GBM disease)

– Lung haemorrhage (anti-GBM, ANCA, lupus)

clinical assessment: intrinsic renal diseaseDiseases of small vessels and glomeruli…

• Haemolytic-uremic syndrome/thrombotic thrombocytopenic:

– Fever, neurologic abnormalities

• Malignant hypertension

– Evidence of damage to other organs:

– headache, papilloedema, heart failure with LVH by echocardiography/ECG

(Typically resolves with blood pressure control)

clinical assessment: intrinsic renal diseaseDiseases of large renal vessels

• Renal artery thrombosis:

– Flank or abdominal pain

• Athero-embloic disease:

– Retinal plaques, palpable purpura, livedo reticularis

• Renal vein thrombosis:

– Flank pain

post-renal causes –obstruction…

acute kidney injury: post-renal (obstruction)• These are mostly urinary tract obstruction

• Ureteric

– They may be bilateral, or unilateral in the case of one kidney

– They include calculi, blood clots, sloughed papillae, cancer, external compression (e.g.. retroperitoneal fibrosis)

• Bladder neck:

– neurogenic bladder, prostatic hypertrophy, calculi, blood clots, cancer

• Urethra:

– stricture or congenital valves

clinical assessment: post-renal (obstruction)

Clinical Assessment

– History of renal stones or prostatic disease

– Palpable bladder, flank or abdominal pain

– Imaging to assess obstruction, including CT scan and/or ultrasound

acute kidney injury: workup

• Several laboratory tests are useful for assessing the aetiology of acute

kidney injury (AKI) and can aid in proper management of the disease:

Examples:

• Full blood count (FBC)

• Serum biochemistries

• Urine analysis with microscopy

• Urine electrolytes

• Glomerular function tests

acute kidney injury: workupurine analysis with microscopy

PRE RENAL RENAL (ATN)

U-[NA] <20 >40

Urinary sediment Hialine casts Red cells / granular cast

U-UREA

S-UREA

>14 <10

OSMOL > 600mOsm/kg +-250-300

SG > 1020 +-1010

FENa <1% >2%

= (uNA/sNA) x (sCR/uCR) x 100

acute kidney injury: workupglomerular function tests

• Creatinine clearance (Cr Cl):

acute kidney injury: complications• Metabolic acidosis

• Hyperkalaemia

• pulmonary oedema

– These may require medical treatment with sodium bicarbonate, shifting potassium, and diuretics

• Lack of improvement with fluid resuscitation,

• therapy-resistant hyperkalaemia,

• metabolic acidosis, or

• fluid overload

– These may necessitate artificial support in the form of dialysis or hemofiltration.

chronickidney

disease

chronic kidney disease

• Chronic kidney disease (CKD) encompasses a spectrum of different

pathophysiologic processes associated with abnormal kidney function,

and a progressive decline in glomerular filtration rate (GFR).

chronic kidney disease: staging

GFR, ml/min

Stage 1 ≥ 90

Stage 2 60-89

Stage 3 30-59

Stage 4 15-29

Stage 5 <15

chronic kidney disease: staging…

• GFR >90 ml/min– HPT is frequent

• GFR 60 – 89 ml/min– HPT frequent, PTH levels start to rise.

• GFR 30 – 59 ml/min– HPT, PTH markedly increased, decreased calcium absorption,

reduced phosphate excretion, onset of anaemia, left ventricular hypertrophy.

• GFR 15 – 29 ml/min– triglyceride start to rise, hyperphosphatemia, metabolic acidosis

with tendency to hyperkalemia.

chronic kidney disease: causes

The three most common causes of CKD are

1. diabetes mellitus

2. Hypertension

3. Glomerulonephritis

Together, these cause approximately 75% of all adult cases.

chronic kidney disease: treatment

The first step in the treatment of chronic kidney disease (CKD) is to

determine the underlying cause

Some causes are reversible, including use of medications that impair

kidney function, blockage in the urinary tract, or decreased blood flow

to the kidneys.

Treatment of reversible causes may prevent CKD from worsening.

chronic kidney disease: treatment…

Hypertension

Hypertension in 80 to 85 % of people with CKD

Maintaining good BP control is the most important goal for trying to

slow the progression of CKD.

angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor

blocker (ARB)

reduces blood pressure and levels of protein in the urine, and is thought

to slow the progression of CKD to a greater extent than some of the

other medicines used to treat high blood pressure.

Sometimes, a diuretic or other medication is also added

chronic kidney disease: treatment…

Anaemia

• People with CKD are at risk for anaemia

(This occurs because improperly functioning kidneys produce reduced

erythropoietin)

• Selected patients can be treated with drugs that stimulate production of

red blood cells. In some cases, iron supplements are also prescribed

chronic kidney disease: treatment…Dietary changes

Changes in diet may be recommended to control or prevent some of the

complications of CKD; most important is salt restriction to help control

the blood pressure.

• Protein

– Restricting protein in the diet may slow the progression of CKD, although

it is not clear if the benefits of protein restriction are worth the difficulty of

sticking to a low protein diet.

chronic kidney disease: treatment…Dietary changes cont.…

• Potassium

– Some people with CKD develop a high blood potassium level, which can interfere

with normal cell function. This is frequently treated with a diuretic. Measures to

prevent high potassium might also be recommended, including a low potassium

diet and avoiding medicines that raise potassium levels

• Phosphate

– Phosphate is a mineral that helps to keep the bones healthy. Early in the course of

CKD, the body begins to retain phosphate. As the disease progresses, high blood

phosphate levels can develop. This is usually treated with medicines that prevent

phosphate (found in foods) from being absorbed in the digestive tract. Dietary

phosphate restrictions are also recommended

chronic kidney disease: treatment…

• Cholesterol and triglycerides

High cholesterol and triglyceride levels are common in people with

kidney disease. High triglycerides have been associated with an

increased risk of coronary artery disease, which can lead to heart attack

• Treatments to reduce the risk of coronary artery disease are usually

recommended, including dietary changes, medications for high

triglyceride and cholesterol levels, stopping smoking, and tight blood

sugar control in people with diabetes.

g l o m e r u l a r d i s e a s en e p h r o t i c s y n d r o m e / s y n d r o m e

glomerular disease: nephrotic syndromeDescription of Nephrotic Syndrome

• It is characterized by:

– an increase in permeability of the capillary walls of the glomerulus

– leading to the presence of high levels of protein passing from the

blood to the urine.

glomerular disease: nephrotic syndrome

Signs and Symptoms

– It is characterized by

– Proteinuria (nephrotic range >3.5g/day)

– Hypoalbuminemia

– Hyperlipidaemia

– Oedema

– Lipiduria can also occur, but is not essential for the diagnosis of nephrotic syndrome.

– Hyponatremia also occur with a low fractional sodium excretion.

glomerular disease: nephrotic syndrome…Treatment

• Corticosteroids (high dose prednisone), cyclophosphamide and

cyclosporine are used to induce remission

• Diuretics are used to reduce oedema

• ACE-inhibitors and Angiotensin II receptor blockers can reduce

proteinuria

glomerular disease: nephrotic syndrome…Complications

These include:

• Thromboembolism (nephrotic

syndrome being hypercoagulable state)

• Infection (increased risk)

• Acute kidney failure

• Pulmonary oedema

• Massive ascites

• Microcytic anaemia

• Protein malnutrition

• Growth retardation

• Vitamin D deficiency

• Cushing’s syndrome

• Hypocalcaemia

glomerular disease: nephritic syndrome (agn)

Description of Nephritic Syndrome (Glomerulonephritis)

• Glomerulonephritis or acute nephritic syndrome

• This is a disorder / inflammation of the glomeruli and is characterized

by:

– Oedema

– High blood pressure

– Haematuria

glomerular disease: diagnosis

Diagnosis of glomerular diseases can be made by:

• Urine tests

• Blood tests –

• Serum albumin, E/U/Cr. CRP/ESR to check for systemic causes

• Imaging tests - Ultrasound

• Kidney biopsy

urine studiesUrinalysis

• Urinalysis is the first test used in the diagnosis of Nephrotic Syndrome

• Nephrotic range proteinuria 3+ or 4+ on dipstick

• Glucosuria points to diabetes

Urine sediment examination

• May show cells and/or casts

• More than 2 granular casts in the entire sediment is a biomarker for renal

parenchymal disease

Urinary protein measurement

• Timed collection over a 24-hour period

• In healthy individuals, there are no more than 150 mg of total protein in a 24-hour

urine collection (as against 3.5g in NS)

glomerular disease: treatment

The treatment of glomerular disease depends on

• the form (acute or chronic)

• the underlying cause

• the severity of associated signs and symptoms.

The goal of Treatment include:

• To relieve symptoms

• To prevent complications

• To delay kidney damage

• Treat underlying cause

• Lifestyle modification

glomerular disease: treatment

• Keep the BP at or below 130/80mmHg

– Aim is to delay kidney damage

– Medications commonly used: ACE-Inhibitors and ARBs.

– These have the added advantage of reducing protein lost in urine.

• Suppress the immune system

– by using corticosteroids (glucocorticoids) and other immune suppressant

medications .

• Treat dyslipidaemias

– to prevent other cardiovascular complications by use of Statins.

glomerular disease: treatment

• Diuretics for the Oedema.

• Antithrombolytic agents to prevent thromboembolism

• Low salt diet and low-protein diets are helpful.

• Some forms of glomerular disease, e.g. those caused by infection,

improve after the infection is treated.

• Treat other complications such as Acute / Chronic Kidney Disease.

Renal Replacement Therapy may be helpful

r e n a l s t o n e s ( n e p h ro l i t h i a s i s )

renal stones (nephrolithiasis)

• Nephrolithiasis refers to calculi in the kidneys.

• Nephroliths are crystal aggregates of dissolved minerals that form in

the kidneys as a result of abnormalities in renal physiology and urine

content

renal stones (nephrolithiasis)…

Causes:• A high concentration of a substance in the urine due to:

– low urine volume.– high excretion rate

• pH changes:– alkaline urine predisposes to Ca deposition (e.g. infection)– acidic urine predisposes to uric acid deposition

• Stagnation, usually due to urinary tract obstruction.

types of stones (or calculi)

4 main chemical types of renal calculi:

1. calcium stones:

• Most kidney stones are calcium compounds.

• May be associated with conditions such as hyperparathyroidism.

• Examples: Ca-oxalate (+ phosphate); ca-phosphate

2. Uric acid stones

• Uric acid stones are formed in about 10% of gouty cases.

• May be associated with low urinary pH due to inadequate buffer

production.

types of stones (or calculi)…

3. Magnesium ammonium phosphate stones (struvite).

• These are often large stones

• They are often associated with infections (eg UTI).

• Occur more commonly in women

4. Rare forms

• cystine: e.g. in cystinuria – arising from transport defect of dibasic

amino acids and cystine.

• xanthine: e.g. in xanthine oxidase deficiency

nephrolithiasis: historical features• Important information in the history include the following:

– Duration, characteristics, and location of pain

– History of urinary calculi

– Prior complications related to stone manipulation

– Urinary tract infections

– Loss of renal function

– Family history of calculi

– Solitary or transplanted kidney

– Chemical composition of previously passed stones

nephrolithiasis: symptoms and signs• The hallmark of stones that obstruct the ureter or renal pelvis is

excruciating, intermittent pain that radiates from the flank to the groin or to the genital area and inner thigh.

• This particular type of pain, known as renal colic, is often described as one of the strongest pain sensations known.

• Renal colic caused by kidney stones is commonly accompanied by urinary urgency, restlessness, haematuria, sweating, nausea, and vomiting.

nephrolithiasis: treatment options

Treatment Options

• These depend on the cause and presentation.

• Options include:

– Acidification of urine

– Antispasmodic medications e.g. hyoscine

– Ureteroscopy

– Pain medications

– Alpha blocker e.g. terazosin and tamsulosin relax the musculature and facilitate passage of the stone

– Good hydration is a good preventive method. Drink water throughout the day.

polyur ia

polyuria

• Polyuria is urine output of > 3L/day.

• Polyuria can be categorized as

– water diuresis in which the urinary osmolality is less than 200 or

– osmotic diuresis when the urinary osmolality is more than 300.

polyuria: calculating osmolality• Osmolality of body fluid is a measure of its solute/water ratio.

• The osmolality of serum, urine, or other body fluids depends on

the number of osmotically active ions and molecules dissolved in a

kilogram of body water.

• Urine osmolality is a more accurate measurement of urine concentration

than specific gravity.

• urine osmolality can be compared with the serum osmolality to obtain a

more accurate picture of a patient's fluid homeostasis.

• serum osmolality = 2 x serum sodium + serum glucose + serum urea (all in

mmol/L)

polyuria: causes

• Polyuria results from any process that involves:

– Sustained increase in water intake (polydipsia)

– Decreased ADH secretion (central diabetic insipidus)

– Decreased peripheral ADH sensitivity (nephrogenic diabetic

insipidus)

– Solute diuresis.

polyuria: causes…

• Water diuresis (urinary osmolality <200mOsm/kg)

– Compulsive water drinking.

– Diabetes insipidus - neurogenic or nephrogenic

• Osmotic diuresis (urinary osmolality +/> 300)

• Caused by the presence of incompletely reabsorbed solutes in the

tubular lumen such as:

– Na+: dietary, iatrogenic, diuretics, salt-losing nephritis.

– Urea: CRF, recovery phase of acute tubular necrosis or post-renal failure.

– Glucose: (diabetes mellitus).

– Mannitol and some other therapeutic agents.

polyuria: causes…

• The most common cause of polyuria in both adults and children is uncontrolled diabetes mellitus causing an osmotic diuresis

• In the absence of diabetes mellitus, the most common cause are primary polydipsia (excessive fluid drinking), central diabetes insipidus and nephrogenic diabetes insipidus.

• Polyuria may also be due to various chemical substance (diuretics, caffeine, alcohol)

• It may also occur after supraventricular tachycardias, during an onset of atrial fibrillation, childbirth, and the removal of an obstruction within the urinary tract. Diuresis is restrained by antidiuretics such as ADH, angiotensin II and aldosterone

renal acidosis

renal acidosis

• Renal tubular acidosis is acidosis and electrolyte disturbances due to

failure of the kidney to appropriately acidify the urine.

• This can be due to:

– impaired hydrogen ion excretion (type 1)

– impaired bicarbonate reabsorption (type 2) or

– abnormal aldosterone

renal acidosis…

• 2 components to H+ excretion by the kidney:

– reabsorption of filtered bicarbonate in the proximal tubule

– H+ secretion in the distal tubule.

uraemic acidosis

1. uraemic acidosis.

• Seen in acute or chronic renal failure when there is decreased H+

excretion due to both glomerular and tubular failure.

• Acidosis develops only when the GFR falls below about 20 ml/min.

(plasma creatinine >350mmol/l).

• Usually it is associated with hyperkalaemia.

renal tubular acidosis rta

2. renal tubular acidosis (rta)

• Tubular dysfunction, with normal or perhaps slightly decreased

glomerular function.

• The urine pH is often inappropriately high in the face of the systemic

acidosis.

• Type 1 – distal

• Type 2 – proximal

type 1 (distal) rta

i. Type 1 (distal) RTA

• Due to inability of distal nephron to excrete H+.

• The urine pH is inappropriately high (pH > 5.5),

• Associated with hypokalaemia, nephro-calcinosis and rickets.

• Hyperchloremic metabolic acidosis

• Hypokalaemia occurs because there is an increase in K+/Na+ exchange

compensating for the defect in H+/Na+ exchange in the distal tubule.

type 1 (distal) rta: clinical manifestation• Confusion/ decreased alertness

• Fatigue

• Acidotic breathing

• Impaired growth in children

• Muscle weakness

• Kidney stones

• Nephrocalcinosis

• Osteomalacia (renal rickets)

type 2 (proximal) rta

ii. Type 2 (proximal) RTA

• Due to defective proximal bicarbonate reabsorption.

• Urine pH can be appropriately acidic (< 5.5) since distal tubular H+

excretion is normal.

• Associated with hypokalaemia, due to the increased delivery of Na+ to

the distal tubule where Na+/K+ exchange occurs

• Proximal RTA may be isolated or may be associated with other proximal

tubular defects: glycosuria, phosphaturia and amino aciduria – i.e. the

Fanconi syndrome.

• Can be genetic (e.g. with cystinosis) or acquired (e.g. toxins).

management: renal acidosis

• The goal is to restore normal acid and electrolytes in the body

• This will correct the bone disorders and calcium build-up in the kidneys

(nephrocalcinosis and kidney stones.

• The underlying cause of (distal) rta should be corrected if it can be

identified

• Medication include: the use of alkali such as alkaline such as potassium

citrate and sodium bicarbonate

hiv-associated nephropathy (hivan)

hiv- associated nephropathy (hivan)

• Renal disease is a relatively common complication in patients with human immunodeficiency virus (HIV) disease.

• it is a leading cause of end stage kidney disease among the HIV-1 seropositive population.

• HIV nephropathy can result from direct kidney infection with HIV or from the adverse effects of antiretroviral drugs

• It manifests as AIDS-defining late-stage illness (CD4 <200) or during the acute HIV infection

• Patients with HIV disease are at risk for developing prerenal azotemia due to volume depletion resulting from salt wasting, poor nutrition, nausea, or vomiting.

hiv- associated nephropathy (hivan)…HIV-associated nephropathy (HIVAN) is characterized by the following

findings:

• Nephrotic range proteinuria

• Azotemia – abnormally high levels of nitrogen-containing compounds

(urea, creatinine, various body waste compounds, and other nitrogen-

rich compounds)

• Normal to large kidneys on ultrasound images

• Normal blood pressure

• Histologically, it is an aggressive collapsing Focal segmental

glomerulosclerosis (FSGS) – renal biopsy findings

hivan: approach to treatment

• HAART

– Consider ABC/3TC

– Avoid potentially nephrotoxic ARVs like TDF (glomerular & tubular

toxicity)

• ACE-Inhibitors / ARBs

– Maintain BP <130/80mmHg

– Antiproteinuric and renoproteective effect (these are independent of

antihypertensive effect)

– But may worsen hyperkalemia

hivan: approach to treatment…

• Corticosteroids

– Corticosteroid therapy can rapidly but transiently reverse HIVAN and

make patients less dialysis dependent.

– Dosage: Prednisone 1mg/kg (up to 80 mg for 2 months, then tapered

for 2-4 months)

• Monitor E/U/Cr and Urine protein/creatinine ratio

• Some reports on paediatric populations suggest that cyclosporine can be

effective in reducing proteinuria in persons with HIVAN.

• Patients who progress to end-stage renal disease (ESRD) require dialysis

and consideration of renal transplantation in carefully selected cases.

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