Renal insufficiency
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Renal Insufficiency. “To be a great champion you must believe you are the best. If you’re not, pretend you are….!” – Muhammad Ali. TOPICS. Introduction Acute renal failure Chronic renal failure Uremia. Functions of kidney.

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Renal insufficiency

Renal Insufficiency


Renal insufficiency

To be a great champion you must believe you are the best. If youre not, pretend you are.! Muhammad Ali


Topics

TOPICS

  • Introduction

  • Acute renal failure

  • Chronic renal failure

  • Uremia


Functions of kidney

Functions of kidney

The kidneys are a pair of small organs that lie on either side of your spine at about waist level. They act as filters that keep your blood free of by-products and toxins.

  • The kidneys excrete these compounds with water to make urine.

  • They also eliminate excess body water while selectively reabsorbing useful chemicals and allowing waste to pass freely into the bladder as urine.

  • They allow you to continue to consume a variety of foods, drugs, vitamins and supplements, additives, and excess fluids without worry that toxic by-products will build up to harmful levels.


Renal insufficiency

  • The kidneys play an essential role in maintaining electrolyte and acid-base balance.

  • They produce some hormones including renin, prostaglandins, erythropoietin, and active vitamin D.

  • So, they are crucial in the regulation of blood pressure, formation of matured red blood cells, and metabolism of calcium and phosphorus.


Functions of the kidney

Functions of the Kidney

  • Waste excretion

  • Electrolyte balance

  • Fluid balance

  • pH

  • Osmolality

  • Hormone production


Renal insufficiency

Anatomy of Kidney


Manifestation of renal dysfunction

Manifestation of renal dysfunction

  • Glomerulus

    decreasedGFR

    glomerular filtration membrane permeability alteration

  • Renal tubule

    concentrative function decline (hyposthennuria/isosthennuria)

    water, electrolyte, acid-base disorder

    others

  • Endocrine disorder

    hypertension anemia renal osteodystrophy

    others


Vitd 3

VitD3

25- 1-

7- VitD3 25-(OH)VitD3 1,25-(OH) 2VitD3


Acute renal failure arf

Acute Renal Failure, ARF


Renal insufficiency

  • Definition

  • Etiology & classification

    Prerenal failure

    Intrinsic renal failure

    Post(obstructive) renal failure

  • Pathogenesis

  • Clinical manifestation

  • Therapy


Definition

Definition

  • Acute renal failure (ARF) is defined as a precipitous and significant (>50%) decrease in glomerular filtration rate (GFR) over a period of hours to days, with an accompany-ing accumulation of nitrogenous wastes in the body.


Renal insufficiency

acute renal failureARF

GFR

400ml400ml


Etiology

Etiology

  • Pre-renal (~70% of cases)

    resulting from impaired blood flow to or oxygenation of the kidneys.

  • Intrinsic-renal (~25% of cases)

    resulting from injury to or malformation of kidney tissues.

  • Post-renal (<5% of cases)

    resulting from obstruction of urinary flow between the kidney and urinary meatus.


Causes

Causes

  • Prerenal failure - Diseases that compromise renal perfusion

  • Decreased effective arterial blood volume - Hypovolemia, CHF, liver failure, sepsis

  • Renal arterial disease - Renal arterial stenosis (atherosclerotic, fibromuscular dysplasia), embolic disease (septic, cholesterol)


Renal insufficiency

ADHAld

GFR


Renal insufficiency

  • Intrinsic renal failure - Diseases of the renal parenchyma, specifically involving the renal tubules, glomeruli, interstitium

  • ATN, ischemia, toxins (eg, aminoglycosides, radiocontrast, heme pigments, cisplatin, myeloma light chains, ethylene glycol)

  • Interstitial diseases - Acute interstitial nephritis, drug reactions, autoimmune diseases (eg, systemic lupus erythematosus [SLE]), infiltrative disease (sarcoidosis, lymphoma), infectious agents (Legionnaire disease, hantavirus)

  • Acute glomerulonephritis

  • Vascular diseases - Hypertensive crisis, polyarteritis nodosa, vasculitis


Renal insufficiency

  • Postrenal failure - Diseases causing urinary obstruction from the level of the renal tubules to the urethra

  • Tubular obstruction from crystals (eg, uric acid, calcium oxalate, acyclovir, sulfonamide, methotrexate, myeloma light chains)

  • Ureteral obstruction - Retroperitoneal tumor, retroperitoneal fibrosis (methysergide, propranolol, hydralazine), urolithiasis, papillary necrosis

  • Urethral obstruction - Benign prostatic hypertrophy; prostate, cervical, bladder, colorectal carcinoma; bladder hematoma; bladder stone; obstructed Foley catheter; neurogenic bladder.


Renal insufficiency

Causes of ARF in tertiary care hospital setting


Renal insufficiency

  • ARF ARF

    ARF

  • ARFARF

    acute tubular necrosisATNARFARF75%80%

  • ARF


Pathogenesis of arf

Pathogenesis of ARF

  • Decreased renal blood flow

    Renal hypoperfusion

    Vasoconstriction

    Vascular obstruction

  • Redistribution of renal blood flow

I. Renal hemodynamics factors


Renal insufficiency

II. Nephronal factors

  • Tubule injury

    Tubule obstruction

    Passive backflow


Renal insufficiency

Acute Renal Failure, IntrinsicAcute Tubular Necrosis

  • Renal hypoperfusion/ischemia

  • Nephrotoxic agents (both endogenous and exogenous)

  • Mortality 50%

    • Bronchopulmonary infections, sepsis, cardiovascular disease, bleeding disorders

  • Complete Recovery 25%, Incomplete 20%, No Recovery 5%


Renal insufficiency

Acute Tubular NecrosisNephrotoxic Agents

  • Exogenous

  • Antibiotics

  • Contrast

  • Diuretics

  • Chemotherapeutics

  • Analgesics

  • Solvents, metals, chemicals

  • HIV meds

  • Antiulcer meds

  • Anesthetics

  • Endogenous

  • Pigment nephropathy

  • Crystal deposition

  • Tumor-specific syndromes


Renal insufficiency

Acute Tubular Necrosis

Cell Hypoxia

Depletion of ATP

Hypoxanthine

Impaired function

Of plasma membranes

And ATPases

Ca++ imbalance

Na-K imbalance

Cell Swelling

Disrupt cytoskeleton

Activate phospholipases

Formation of xanthine oxidase

Uncoupling of oxidative phosphorylation

Disrupt lipid

bilayer

Reperfusion injury

Free radicals


Renal insufficiency

Acute Tubular Necrosis

  • Leads to

  • Loss of cell polarity

  • Brush border loss

  • Impaired cell-cell adhesion

  • Impaired tight junction

  • End results

  • Impaired solute and water transport

  • Sloughing of tubule cells obstruction

  • Back leakage of filtrate


Renal insufficiency

GFR


Characteristics clinical courses

Characteristics & clinical courses

  • Oliguric phase

  • Diuretic phase

  • Recovery phase


Oliguric phase

Oliguric phase

Usually lasting for 1 to 6 weeks,the average duration is between 7 & 10 days.

  • Features of urine: I. Oliguria or Anuria

    II. Hematuria and casts

    III. Low specific gravity and osmolality

    IV. Urinary [Na+] above 20mM

  • Azotemia

  • Metabolic acidosis

  • Hyperkalemia

  • Hypervolemia / Hypertension

  • Others: edema, water intoxicationtachypnea


Renal insufficiency

Urinary Indices in ARF


Renal insufficiency

ATN

/

>1.020 <1.015

>500mOsm/L <400mOsm/L

<20mmol/L >40mmol/L

>40 <20

GFR


Renal insufficiency

Muddy Brown Cast


Renal insufficiency

Red Cell Cast


Renal insufficiency

White Cell Casts


Diuretic phase

Diuretic phase

As healing begins, improvement is reflected in the production of more than 400 ml of urine per day.

  • Fluid and electrolyte abnormalities.

  • Cr may still rise for 1-2 more days.

Recovery phase


Renal insufficiency

ARF

1.

2.GFR28.6mmol/L40mg/dl

3.ARF

4.GFRARF

5.GFR


Renal insufficiency

400mlGFR


Nonoliguric acute renal failure

Nonoliguric acute renal failure

ARF 4001000 ml/dARFARFARFARF


Management

Management

  • Renal Diet

  • Acidosis

  • Hyperuricemia

  • Hypertension

  • Volume overload

  • Protein Load

  • Newer AgentsANF

  • Dialysis

  • Kidney Transplantation

    Hospital inpatients with ARF ~50% mortality rate


Dialysis indications

Dialysis indications

I. Serum abnormalities unresponsive to medical therapy

  • Severe Acidosis

  • Severe Hyperkalemia

    II. Uremia

  • Mental status changes (usually delirium)

  • Nausea and vomiting

  • Pericarditis (pericardial friction rub)

    III. Volume Overload


Renal insufficiency

Peritoneal Dialysis


Renal insufficiency

Hemodialysis

  • Blood is circulated through artificial cellophane membrane that permits a similar passage of water and solutes


Chronic renal failure crf

Chronic Renal Failure, CRF


Renal insufficiency

  • Definition

  • Etiology

  • Pathogenesis

  • Clinical manifestation

  • Therapy


Renal insufficiency

Definition

  • Chronic renal failure (CRF) is defined as a permanent reduction in glomerular filtration rate (GFR) sufficient to produce detectable alterations in well-being and organ function. This usually occurs at GFR below 25 ml/min.


Renal insufficiency

  • CRF is characterized by progressive and irreversible loss of large numbers of functioning nephrons. Serious clinical symptoms often do not occur until the number of functional nephrons falls to at least 70 per cent below normal. In fact relatively normal blood concentrations of most electrolytes and normal body fluid volumes can still be maintained until the number of functioning nephrons decreases below 20-30percent of normal.


Renal insufficiency


Causes of crf

Causes of CRF

Any disorder that permanently destroys nephrons can result in chronic renal failure. Most common causes of CRF are:

  • Diabetic nephropathy

  • Hypertensive nephrosclerosis

  • Glomerulonephritis

  • Interstitial nephritis

  • Polycystic kidney disease


Renal insufficiency

CRF50%60%

1

2

3

4

5


Clinical courses of crf

Clinical courses of CRF

Four stages of decreased renal function may be visualized:

  • Silent GFR up to 50 ml/min.

  • Renal insufficiency GFR 25 to 50 ml/min.

  • Renal failure GFR 5/10 to 25 ml/min

  • End-stage renal failure (ESRF) GFR less than 5/10 ml/min.


Renal insufficiency

Stage

Description

GFR Level

Normal kidney function

Healthy kidneys

90 mL/min or more

Stage 1

Kidney damage with normal or high GFR

90 mL/min or more

Stage 2

Kidney damage and mild decrease in GFR

60 to 89 mL/min

Stage 3

Moderate decrease in GFR

30 to 59 mL/min

Stage 4

Severe decrease in GFR

15 to 29 mL/min

Stage 5

Kidney failure

Less than 15 mL/min or on dialysis

Stages of Chronic Kidney Disease


Renal insufficiency

ml/min

>50

20-50

10-20

<10


Pathogenesis

Pathogenesis

  • The most intriguing aspect of CRF is that compensatory mechanisms allow loss of 90% of GFR before manifestations of the uremic syndrome are evident. Thus a variety of adaptations compensate for the decreased GFR and allow a new steady state of external balance to exist, but on the other hand contribute to the uremic syndrome. In spite of these adaptations, the hallmark of CRF is the loss of flexibility in responding to challenges to external load of solutes and water.

    Intact Nephron hypothesisTubulointerstitial cell injury

    Trade-off hypothesis


Intact nephron hypothesis

Intact Nephron Hypothesis

  • Nephrons functioning in diseased kidneys maintain glomerulo-tubular balance. That is, filtration and net excretion of various substances are coordinated. (e.g. with normal renal function, usually 50-60% of filtered urea is reabsorbed from the tubules. In CRF it may fall to 30% to maintain balance).


The magnification phenomenon

The Magnification Phenomenon

  • although nephrons in diseased kidneys function homogeneously, they alter their handling of given solutes as needed to maintain balance of these solutes. That is, nephrons can magnify their excretion of a given solute. (e.g. tubular creatinine excretion is < 10% with normal renal function. In CRF it may increase to 30%).


Trade off hypothesis

Trade-off Hypothesis

  • The mechanisms that are magnified to maintain individual solute control may have deleterious effects on other systems. This trade-off is seen in the increased parathyroid hormone (PTH) secretion seen in CRF which enhances renal phosphorus excretion. PTH has been implicated in the pathogenesis of many disturbances of uremia (sleep, sex, bone, disease, anemia, lipidemia, vascular disease). As renal disease progresses and GFR decreases, high level PTH no longer maintains the phosphate excretion. The excessive PTH may result in further side effects, such as osteomalacia, deposit of calcium phosphate salts into soft tissue and damage of cardiovascular, neural systems.


Renal insufficiency

  • -


Renal insufficiency

GFR GFR VitD3

PTH


Renal insufficiency

[ ] /

Ccr =

[ ]

*90140ml/min

*23

*<40g/


Renal insufficiency

Clinical manifestations of CRF

  • Loss of nephrons function to excrete water and solutes.

  • Characteristics of urine:

  • urine volume,osmotic & gravity, urinary sediment

  • Effects on body fluids.

  • water & sodium imbalance

  • potassium imbalance

  • metabolic acidosis

  • phosphate & calcium metabolism dysfunction

  • azotemia

  • Other signs of CRF

  • cardiovascular abnormalities

  • anemia & bleeding

  • renal osteodystrophy


Anemia

Anemia

Anemia is universal as GFR falls below 25 ml/min.; in certain disorders it may occur with mild renal insufficiency. Several factors contribute:

a. Erythropoiesis is markedly depressed, mainly due to reduced erythropoietin production; in addition, there may be reduced end-organ response to erythropoietin with reduced heme synthesis.

b. Red cell survival is shortened with a mild to moderate decrease in red cell life span, possible due to a uremic toxin.

c. Blood loss is common in uremic patients, possibly secondary to abnormal coagulation due to decreased platelet function.

d. Marrow space fibrosis occurs with osteitis fibrosa of secondary hyperparathyroidism resulting in decreased erythropoiesis.


Hypertension

Hypertension

Hypertension occurs in 80% to 90% of patients with renal insufficiency. Several factors contribute:

a. Expansion of extracellular fluid volume; this may arise because of reduced ability of the kidney to excrete ingested sodium.

b. Increased activity of the renin-angiotensin system is common; many patients with advanced renal failure have renin levels that are not completely suppressed by the elevated blood pressure.

c. Dysfunction of the autonomic nervous system occurs with insensitive baroreceptor sensitive and with increased sympathetic tone.

d. Possible diminished presence of vasodilators: there may be decreased renal generation of prostaglandins or of factors in the kallikrein-kinin system.


Altered calcium and phosphorus metabolism renal osteodystrophy

Altered Calcium and Phosphorus Metabolism (Renal Osteodystrophy)

a. As GFR decreases there is a slight retention of phosphorus; this phosphorus retention can lead to hypocalcemia, which stimulates PTH. The latter causes phosphaturia, with restoration of serum phosphorus and calcium toward normal. However, this occurs only at the expense of elevated serum PTH levels. This cycle repeats itself in progressive renal failure with PTH levels increasing progressively. Ultimately, the renal tubule can no longer respond to higher levels of PTH with a further decrease in phosphorus reabsorption. When this occurs, hyperphosphatemia develops, hypocalcemia may become prominent and PTH level can increase to very high levels. High PTH levels cause bone disease with severe osteitis fibrosa.

b. Altered vitamin D metabolism occurs secondary to decreased renal mass or to phosphate retention, with decreased synthesis of 1,25 (OH)2 D3. This deficiency leads to: 1. Diminished intestinal absorption of calcium, 2. decreased calcemic response of the skeleton to PTH, 3. impaired suppression of PTH secretion for any increase in serum calcium level, and 4. altered collagen synthesis. With advanced renal failure, these events can lead to secondary hyperparathyroidism and osteomalacia.

c. Skeletal resistance to the calcemic action of PTH develops; thus an increased PTH is required to maintain serum calcium at any level.

d. Finally, accumulation of aluminum from aluminum binding antacids may contribute to the bone disease.


Renal insufficiency

1

2

3

4renal hypertension

5renal anemia

6

7


Renal insufficiency

GFR

Ald II

PGA2PGE2


Renal insufficiency

1,25-(OH)2VitD3 GFR

PTH


Uremia

Uremia


Concept

Concept

  • Uremia, from the Greek urine in the blood, is a clinical and biochemical syndrome that occurs either abruptly or gradually as renal function decreases acutely or chronically. In its extreme expression as uremic coma, the patient behaves as if poisoned, hypothermia, intermittent seizures, a bleeding diathesis,cardiac arrhythmias, vomiting, and rapid, shallow respirations may appears.


Uremia1

Uremia

  • Definition: symptomatic azotemia

  • Acidosis ( tachypnea)

  • Mental Status changes

  • Hypervolemia / Hypertension

  • Hyperkalemia

  • Pericarditis


Renal insufficiency

uremia


Clinical manifestations

Clinical Manifestations

The symptoms and signs which constitute the uremic syndrome are summarized below:

  • Neurological Disorders: Fatigue, lethargy, sleep disturbances, headache, seizures, encephalopathy, peripheral neuropathy including restless leg syndrome, paraesthesia, motor weakness, paralysis.

  • Hematologic Disorders: Anemia, bleeding tendency due in part to platelet dysfunction.

  • Cardiovascular Disorders: Pericarditis, hypertension, congestive heart failure, coronary artery disease, myocardiopathy.

  • Pulmonary Disorders: Pleuritis, uremic lung.

  • Gastrointestinal Disorders: Anorexia, nausea, vomiting gastroenteritis, GI bleeding, peptic ulcer.


Renal insufficiency

  • Metabolic-Endocrine Disorders: Glucose intolerance, hyperllipidemia, hyperuricemia, malnutrition, sexual dysfunction and infertility.

  • Bone, Calcium, Phosphorus Disorders: Hyperphosphatemia, hypocalcemia, tetany, metastatic calcification, secondary hyperparathyroidism, 1,25-dihydroxy vitamin D deficiency, osteomalacia, osteitis fibrosa, osteoporosis, osteosclerosis.

  • Skin Disorders: Pruritus, pigmentation, easy bruising, uremic frost.

  • Psychological Disorders: Depression, anxiety, denial, psychosis.

  • Fluid and Electrolyte Disorders: Hyponatremia, hyperkalemia, hypermagnesemia, metabolic acidosis, volume expansion or depletion


Principles of treatment for crf uremia

Principles of treatment for CRF & Uremia

  • Conservative management

  • Dialysis

    Peritoneal dialysis

    Hemodialysis

  • Renal transplantation


Renal insufficiency

case

  • 853100ml/d,480mol/L178mol/L 100mmol/L20mmol/L 1.008


Treatment of end stage renal failure esrf

Treatment of end stage renal failure(ESRF)

  • When GFR falls below 5 ml/min, the patient usually can not live without renal replacement therapy. Renal replacement therapy includes dialysis and kidney transplantation .

  • Various social or medical factors influence decisions about peritoneal or hemodialysis, and transplantation in the treatment of end-stage renal failure. It should also be noted that none of the above are panaceas and each, modality is associated with complications and failures.


Renal insufficiency

  • Azotemia - elevated blood urea nitrogen (BUN >28mg/dL) and creatinine (Cr>1.5mg/dL)

  • Uremia - azotemia with symptoms or signs of renal failure

  • End Stage Renal Disease (ESRD) - uremia requiring transplantation or dialysis

  • Chronic Renal Failure (CRF) - irreversible kidney dysfunction with azotemia >3 months

  • Creatinine Clearance (CCr) - the rate of filtration of creatinine by the kidney (GFR marker)

  • Glomerular Filtration Rate (GFR) - the total rate of filtration of blood by the kidney


Renal insufficiency

The End


Glomerural filtration rate gfr

glomerural filtration rateGFR

  • =


Renal insufficiency

Glomerular Filtration Rate

GFR = Kf [(Pgc-PB) - (gc-B)] = Kf (P-)

Kf = glomerular ultrafiltration coefficient

Pgc = glomerular capillary hydraulic pressure

PB = Bowmans space hydraulic pressure

gc = glomerular colloid osmotic pressure

B = Bowmans space colloid osmotic pressure


Renal insufficiency

Estimates of GFR

  • Inulin neither secreted or reabsorbed

  • Clearance of inulin approximates GFR

  • [U]inulin V

  • [P]inulin

  • Creatine is secreted, so Cr clearance overestimates GFR

GFR =


Renal insufficiency

Estimates of GFR

  • Urinary Estimate

  • [U]cr V

    • [P]cr

  • Cockcroft Gault Estimate

  • [140-age (yr)][body wt (kg)]

  • 72[Pcr]

  • CrCl =

    CrCl =


    Glomerulus

    Glomerulus


    Renal insufficiency

    Filtration Membrane Electron Micro.

    Capillary Space

    GBM

    Endothelium

    Urinary Space

    Podocyte


    Symptoms of chronic kidney disease

    Symptoms of chronic kidney disease

    • Fatigue and weakness (from anemia or accumulation of waste products in the body)

    • Loss of appetite, nausea and vomiting

    • Need to urinate frequently, especially at night

    • Swelling of the legs and puffiness around the eyes (fluid retention)

    • Itching, easy bruising, and pale skin (from anemia)

    • Headaches, numbness in the feet or hands (peripheral neuropathy), disturbed sleep, altered mental status (encephalopathy from the accumulation of waste products or uremic poisons), and restless legs

    • High blood pressure, chest pain due to pericarditis (inflammation around the heart)

    • Shortness of breath from fluid in lungs

    • Bleeding (poor blood clotting)

    • Bone pain and fractures

    • Decreased sexual interest and erectile dysfunction


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