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![acute kidney injury: workup
urine 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](https://image.slidesharecdn.com/disordersofrenalfunction-211120073339/75/Disorders-of-Renal-Function-36-2048.jpg)
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Similar to Disorders of Renal Function
Disorders of Renal Function
- 1.
- 2. outline • anatomy andphysiology • disorders of the renalsystem • acute kidney injury • chronic kidney disease • glomerular disease • nephrolithiasis • polyuria • renal acidosis • hiv-associated nephropathy
- 3. the kidney: an atomy an d p hysio lo g y
- 5. anatomy of thekidneys • 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.
- 6. anatomy of thekidneys… • 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
- 7. the nephron Histologically, The functionalrenal 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)
- 8.
- 9. the renal corpuscle •This consists of glomerulus and bowman capsule
- 10. functions of thekidneys • 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 aminoacids • Hormonal functions via erythropoietin, calcitriol, and vitamin D activation
- 11.
- 12. disorders of the renalsystem
- 13. disorders of therenal 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
- 14.
- 15. acute kidney injury •Acute Kidney Injury (AKI), (previously Acute Renal Failure ARF), is defined as an abrupt decline inthe 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.
- 16. 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
- 17. acute kidney injury:causes…
- 18.
- 19. 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
- 20. 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
- 21. clinical assessment: pre-renalarf 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
- 22.
- 23. intrinsic arf 1. Renovascularobstruction 2. Diseases of the glomeruli or vasculature 3. Acute tubular necrosis 4. Interstitial nephritis 5. Intratubular obstruction
- 24. 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
- 25. acute kidney injury:intrinsic renal causes… 2. Diseases of the glomerulior vasculature • Glomerulonephritis or vasculitis • Others: thrombotic micro-angiopathy, malignant hypertension, collagen vascular diseases (SLE, scleroderma), DIC, PET
- 26. 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 sepsissyndrome • Toxins: – Exogenous (radiocontrast, antibiotics ,chemotherapy) – Endogenous (rhabdomyolysis, haemolysis )
- 27. 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
- 28. acute kidney injury:intrinsic renal causes… 5. Intratubular obstruction • Endogenous: – myeloma proteins, uric acid (tumor lysis syndrome), systemic oxalalosis • Exogenous: – acyclovir, gancyclovir, methotrexate, indinavir
- 29. clinical assessment: intrinsic renaldisease 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)
- 30. clinical assessment: intrinsic renaldisease Diseases 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)
- 31. clinical assessment: intrinsic renaldisease Diseases of large renalvessels • Renal artery thrombosis: – Flank or abdominal pain • Athero-embloic disease: – Retinal plaques, palpable purpura, livedo reticularis • Renal vein thrombosis: – Flank pain
- 32.
- 33. acute kidney injury:post-renal (obstruction) • These are mostly urinary tractobstruction • 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
- 34. clinical assessment: post-renal (obstruction) ClinicalAssessment – History of renal stones or prostatic disease – Palpable bladder, flank or abdominal pain – Imaging to assess obstruction, including CT scan and/or ultrasound
- 35. 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
- 36. acute kidney injury:workup urine 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
- 37. acute kidney injury:workup glomerular function tests • Creatinine clearance (Cr Cl):
- 38. 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 fluidresuscitation, • therapy-resistant hyperkalaemia, • metabolic acidosis, or • fluid overload – These may necessitate artificial support in the form of dialysis or hemofiltration.
- 39.
- 40. 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).
- 41. 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
- 42. 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, decreasedcalcium absorption, reduced phosphate excretion, onset of anaemia, left ventricular hypertrophy. • GFR 15 – 29 ml/min – triglyceride start to rise, hyperphosphatemia, metabolicacidosis with tendency to hyperkalemia.
- 43. 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.
- 44. 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.
- 45. 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 ofCKD. 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
- 46. 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
- 47. chronic kidney disease: treatment… Dietarychanges 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.
- 48. chronic kidney disease: treatment… Dietarychanges 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 arealso recommended
- 49. 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.
- 50. g ne l p o h m ro t e ic ru sy l n a d r ro d me is / ea se s y n d r o m e
- 51. glomerular disease: nephrotic syndrome Descriptionof 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.
- 52. glomerular disease: nephrotic syndrome Signsand 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.
- 53. 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
- 54. glomerular disease: nephrotic syndrome… Complications Theseinclude: • 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
- 55. 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
- 56. glomerular disease: diagnosis Diagnosisof 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
- 57. urine studies Urinalysis • Urinalysisis 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/orcasts • 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)
- 58. glomerular disease: treatment Thetreatment of glomerular disease depends on • the form (acute or chronic) • the underlying cause • the severity of associated signs and symptoms. The goal of Treatmentinclude: • To relieve symptoms • To prevent complications • To delay kidney damage • Treat underlying cause • Lifestyle modification
- 59. 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.
- 60. 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 infectionis treated. • Treat other complications such as Acute / Chronic Kidney Disease. Renal Replacement Therapy may be helpful
- 61. renal sto nes (nephrolithiasis)
- 62. 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
- 63. 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.
- 64. types of stones(or calculi) 4 main chemical types of renalcalculi: 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.
- 65. 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 inwomen 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
- 66. nephrolithiasis: historical features • Importantinformation 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
- 67. 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.
- 68. 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.
- 69.
- 70. polyuria • Polyuria isurine 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.
- 71. polyuria: calculating osmolality • Osmolalityof 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)
- 72. polyuria: causes • Polyuriaresults 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.
- 73. polyuria: causes… • Waterdiuresis (urinary osmolality <200mOsm/kg) – Compulsive water drinking. – Diabetes insipidus - neurogenic ornephrogenic • Osmotic diuresis (urinary osmolality +/> 300) • Caused by the presence of incompletely reabsorbed solutes in the tubular lumen such as: – Na+: dietary, iatrogenic, diuretics, salt-losingnephritis. – Urea: CRF, recovery phase of acute tubular necrosis or post-renal failure. – Glucose: (diabetes mellitus). – Mannitol and some other therapeutic agents.
- 74. polyuria: causes… • Themost 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
- 75.
- 76. renal acidosis • Renaltubular 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
- 77. renal acidosis… • 2components to H+ excretion by the kidney: – reabsorption of filtered bicarbonate in the proximal tubule – H+ secretion in thedistal tubule.
- 78. uraemic acidosis 1. uraemicacidosis. • 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.
- 79. renal tubular acidosisrta 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
- 80. 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.
- 81. type 1(distal) rta:clinical manifestation • Confusion/ decreased alertness • Fatigue • Acidotic breathing • Impaired growth in children • Muscle weakness • Kidney stones • Nephrocalcinosis • Osteomalacia (renal rickets)
- 82. type 2 (proximal)rta ii. Type 2 (proximal) RTA • Dueto 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 RTAmay 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).
- 83. 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
- 84.
- 85. 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.
- 86. hiv- associated nephropathy (hivan)… HIV-associatednephropathy (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
- 87. hivan: approach totreatment • 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
- 88. hivan: approach totreatment… • Corticosteroids – Corticosteroid therapy can rapidly but transiently reverse HIVAN and make patients less dialysisdependent. – 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.
- 89.