This document discusses reversible pre-renal acute renal failure and established acute renal failure. It defines the pathophysiology, clinical features, diagnosis, and management of both conditions. The key points are:
1. Reversible pre-renal acute renal failure is caused by reduced renal perfusion and blood flow. It is diagnosed based on a compatible history, clinical findings of hypotension, and urine osmolality >600 mOsm/kg and sodium <20 mmol/L. Treatment involves restoring blood volume and correcting the underlying cause.
2. Established acute renal failure can develop from severe or prolonged pre-renal injury and is characterized by acute tubular necrosis. Features include oliguria, ur
Acute kidney failure happens when your kidneys suddenly lose the ability to eliminate excess salts, fluids, and waste materials from the blood. Acute kidney failure is also called acute kidney injury or acute renal failure. It's common in people who are already in the hospital. It may develop rapidly over a few hours.
Acute kidney failure happens when your kidneys suddenly lose the ability to eliminate excess salts, fluids, and waste materials from the blood. Acute kidney failure is also called acute kidney injury or acute renal failure. It's common in people who are already in the hospital. It may develop rapidly over a few hours.
Disorders of the renal functions, including anatomy and physiology, acute kidney injury, chronic kidney disease, glomerular disease, nephrolithiasis, polyuria, renal acidosis and HIV-associated nephropathy (HIVAN).
Disorders of the renal functions, including anatomy and physiology, acute kidney injury, chronic kidney disease, glomerular disease, nephrolithiasis, polyuria, renal acidosis and HIV-associated nephropathy (HIVAN).
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
2. • The renal tubules are intact and become hyperfunctional;
that is, tubular reabsorption of sodium and water is increased,
partly through physical factors associated with changes in
blood and urine flow and partly through the influence of
angiotensins, aldosterone and vasopressin.
• This leads to the formation of a low volume of urine which is
concentrated (osmolality > 600 mOsm/kg) but low in sodium
(< 20 mmol/l).
• These urinary changes may be absent in patients with
impaired tubular function, e.g. pre-existing renal impairment,
or those who have received loop diuretics
3. Clinical assessment
• Features of the underlying cause
• There may be marked hypotension and signs of poor peripheral
perfusion, such as delayed capillary return.
• Pre-renal ARF may occur without systemic hypotension,
particularly in patients taking NSAIDs or ACE inhibitors .
• Postural hypotension (a fall in blood pressure > 20/10 mmHg
from lying to standing) is a valuable sign of early hypovolaemia.
• The cause of the reduced renal perfusion may be obvious, but
concealed blood loss can occur into the gastrointestinal tract,
following trauma (particularly where there are fractures of the
pelvis or femur) and into the pregnant uterus.
• Large volumes of intravascular fluid are lost into tissues after
crush injuries or burns, or in severe inflammatory skin diseases or
sepsis.
• Metabolic acidosis and hyperkalaemia are often present.
5. MANAGEMENT OF PRE-RENAL ACUTE
RENAL FAILURE:
• Establish and correct the underlying cause of the ARF.
• If hypovolaemia is present, restore blood volume as rapidly as possible
(with blood, plasma or isotonic saline (0.9%), depending on what has been
lost).
• Monitoring of the central venous pressure or pulmonary wedge pressure
as an adjunct to clinical examination may aid in determining the rate of
administration of fluid.
• Critically ill patients may require invasive haemodynamic monitoring to
assess cardiac output and systemic vascular resistance, and the use of
inotropic drugs to restore an effective blood pressure .
• Correct metabolic acidosis.
– Restoration of blood volume will correct acidosis by restoring kidney function.
– Isotonic sodium bicarbonate (e.g. 500 ml of 1.26%) may be used.
6. PROGNOSIS OF PRE-RENAL ACUTE
RENAL FAILURE
• If treatment is given sufficiently early, renal function will
usually improve rapidly; in such circumstances residual renal
impairment is unlikely.
• In some cases, however, treatment is ineffective and renal
failure becomes established
7. ESTABLISHED ACUTE RENAL FAILURE
• Established ARF may develop following severe or
prolonged under-perfusion of the kidney (pre-
renal ARF). In such cases, the histological pattern
of acute tubular necrosis is usually seen.
• Acute tubular necrosis (ATN)
Acute necrosis of renal tubular cells may result
from ischaemia or nephrotoxicity, caused by
chemical or bacterial toxins, or a combination of
these factors.
8. Pathogenesis of ATN
Ischaemic tubular necrosis
• Ischaemic tubular necrosis usually follows a period of shock,
during which renal blood flow is greatly reduced.
• Even when systemic haemodynamics are restored, renal
blood flow can remain as low as 20% of normal, due to
swelling of the endothelial cells of the glomeruli and
peritubular capillaries, and oedema of the interstitium.
• Blood flow is further reduced by vasoconstrictors such as
thromboxane, vasopressin, noradrenaline (norepinephrine)
and angiotensin II, (partly counterbalanced by the release of
intrarenal vasodilator prostaglandins). Thus, in ischaemic ATN
there is reduced oxygen delivery to the tubular cells.
9. • The tubular cells are vulnerable to ischaemia because they
have high oxygen consumption in order to generate energy
for solute reabsorption, particularly in the thick ascending
limb of the loop of Henle.
• The ischaemic insult ultimately causes death of tubular cells ,
which may shed into the tubular lumen causing tubular
obstruction.
• Focal breaks in the tubular basement membrane develop,
allowing tubular contents to leak into the interstitial tissue
and cause interstitial oedema.
10. • Nephrotoxic ATN
• In nephrotoxic ATN a similar sequence occurs, but it is
initiated by direct toxicity of the causative agent to tubular
cells.
• Examples include the aminoglycoside antibiotics, such as
gentamicin, the cytotoxic agent cisplatin, and the antifungal
drug amphotericin B.
11. There are two major histiologic changes that
take place in ATN:
(1) tubular necrosis with sloughing of the
epithelial cells
(2) occlusion of the tubular lumina by casts and
by cellular debris
13. Features of Established ARF
• These reflect the causal condition( cause of ARF), such as
bleeding,dehydration, septicaemia or systemic disease, together with
features of renal failure.
• Alterations in urine volume
Oliguric:
Patients are usually oliguric (urine volume < 500 ml daily).
Anuria :
(complete absence of urine) is rare and usually indicates acute urinary
tract obstruction or vascular occlusion.
Normal or increased (non-oliguric ARF):
In about 20% of cases, the urine volume is normal or increased, but with a
low GFR and a reduction of tubular reabsorption.
Excretion is inadequate despite good urine output, and the plasma urea
and creatinine increase.
14. • Uraemic features include initial anorexia, nausea and
vomiting followed by drowsiness, apathy, confusion, muscle-
twitching, hiccoughs, fits and coma.
,
• Respiratory rate may be increased due to acidosis,
pulmonary oedema or respiratory infection.
Pulmonary oedema may result from the administration of
excessive amounts of fluids relative to low urine output and
because of increased pulmonary capillary permeability.
• Anaemia due to excessive blood loss or haemolysis .
• Bleeding is more likely because of disordered platelet
function and disturbances of the coagulation cascade.
15. • Retention of salt and water
Pulmonary edema, peripheral edema, ascites, pleural effusion
• Spontaneous gastrointestinal haemorrhage
may occur, often late in the illness, although this is less
common with effective dialysis and the use of agents that
reduce gastric acid production.
• Infections ( may be severe )
may complicate ARF because humoral and cellular immune
mechanisms are depressed.
pericarditis
16. Disturbances of water, electrolyte and acid-
base balance
Hyperkalaemia is common, particularly with massive tissue
breakdown, haemolysis or metabolic acidosis
Dilutional hyponatraemia occurs if the patient has continued to
drink freely despite oliguria or has received inappropriate
amounts of intravenous dextrose.
Metabolic acidosis develops unless prevented by loss of
hydrogen ions through vomiting or aspiration of gastric
contents.
Hypocalcaemia, due to reduced renal production of 1,25-
dihydroxycholecalciferol, is common.
18. Management of Established ARF
• Emergency resuscitation
• Hyperkalaemia (a plasma K+ concentration > 6 mmol/l) must be treated
immediately, to prevent the development of life-threatening cardiac
arrhythmias.
• Hypovolaemia must be treated as for reversible pre-renal ARF , with
monitoring of central venous or pulmonary wedge pressure as required.
• Circulating blood volume should be optimised to ensure adequate renal
perfusion .
• In an anuric or volume-overloaded patient, renal replacement therapy
may be required ( dialysis ).
• Patients with pulmonary oedema usually require dialysis to remove
sodium and water.
• Severe acidosis can be ameliorated with isotonic sodium bicarbonate (e.g.
500 ml of 1.26%) if volume status allows.
19. • The underlying cause of the ARF
This may be obvious or revealed by simple initial investigations (e.g.
ultrasound showing urinary tract obstruction). If not, a range of
investigations, including renal biopsy, may be necessary .
• There is no specific treatment for ATN, other than restoring renal
perfusion.
• Intrinsic renal disease may require specific therapy; for example,
immunosuppressive drugs are of value in some causes of rapidly
progressive glomerulonephritis and plasma infusion and plasma
exchange may be indicated in microangiopathic diseases .
• Post-renal' obstruction should be relieved urgently.
• If pelvic or ureteric dilatation is found and not explained by bladder
outlet obstruction, percutaneous nephrostomy is undertaken to
decompress the urinary system .
• With rapid intervention, dialysis can usually be avoided.
20. • Fluid and electrolyte balance
• After initial resuscitation, daily fluid intake should equal urine
output, plus an additional 500 ml to cover insensible losses;
such losses are higher in febrile patients and in tropical
climates.
If abnormal losses occur, as in diarrhoea, additional fluid and
electrolyte replacement is required.
Measurement of fluid intake and urine output is subject to error
so the patient should be weighed daily.
Large changes in body weight, the development of oedema or
signs of fluid depletion indicate that fluid intake should be
reassessed.
Since sodium and potassium are retained, intake of these
substances should be restricted
21. .
Protein and energy intake
In patients in whom dialysis is likely to be avoided, accumulation of
urea is slowed by dietary protein restriction (to about 40 g/day) and by
suppression of protein catabolism by giving as much energy as possible
in the form of carbohydrate.
Patients treated by dialysis may have more dietary protein (70 g protein
daily). It is important to give adequate energy and nitrogen to
hypercatabolic patients (e.g. sepsis, burns).
In some patients, feeding via a nasogastric tube may be helpful.
Parenteral nutrition may be required, especially in critically ill
patients, because of vomiting or diarrhoea, or if the bowel is not
intact.
Infection control
Patients with ARF are at risk of intercurrent infection. Regular clinical
examination and microbiological investigation, as clinically indicated,
are required to diagnose and treat this complication promptly.
22. Drugs
Some drugs such as NSAIDs and ACE inhibitors may
prolong ARF and temporary withdrawal should be
considered.
Many drugs are excreted renally and dose adjustment
may be required in ARF to avoid accumulation.
Renal replacement therapy
This may be required as supportive management in ARF
23. RENAL REPLACEMENT IN ACUTE RENAL
FAILURE ( dialysis )
•The decision to institute RRT is made on an individual basis, taking
account of other aspects of the patient's care.
• Guideline indications are as follows:
Increased plasma urea and creatinine:
•Plasma urea > 30 mmol/l (180 mg/dl) and creatinine > 600 μmol/l
(6.8 mg/dl) are undesirable.
• At lower levels, if there is progressive biochemical deterioration and
particularly if there is little or no urine output, it may be appropriate
to commence dialysis.
.
24. •Hyperkalaemia. A plasma potassium > 6 mmol/l is hazardous.
Elevated plasma potassium can usually be reduced by medical
measures in the short term , but dialysis is often required for
definitive control.
•Metabolic acidosis. This will often occur together with
hyperkalaemia and raise the plasma potassium further.
•Fluid overload and pulmonary oedema. In patients with continued
urine output, this may be controlled by careful fluid balance and
use of diuretics, but in oligo/anuric patients may be an indication
for RRT.
•Uraemic pericarditis/uraemic encephalopathy. These are features
of severe untreated renal failure; they are uncommon in ARF but
are strong indications for RRT.
•Drug resistant GI manifestations ( repeated vomiting )
26. The options for renal replacement therapy in ARF
are :
Haemodialysis
High-volume haemodialysis
Continuous arteriovenous or venovenous haemofiltration
Peritoneal dialysis
27. Recovery from ARF
• Fortunately, tubular cells can regenerate and re-form the
basement membrane.
• If the patient is supported during the regeneration phase, kidney
function usually returns.
During recovery some patients, primarily those with ATN or after
relief of chronic urinary obstruction, develop a 'diuretic phase in
which urine output increases rapidly and remains excessive for
several days before returning to normal.
This is due in part to loss of the medullary concentration gradient,
which normally allows concentration of the urine in the collecting
duct.
28. • Fluid should be given to replace the urine output as
appropriate.
• Supplements of sodium chloride, sodium bicarbonate
and potassium chloride, and sometimes calcium,
phosphate and magnesium, may be needed to
compensate for increased urinary losses.
• After a few days urine volume falls to normal as the
concentrating mechanism and tubular reabsorption are
restored.
• Not all patients have a diuretic phase, depending on the
severity of the renal damage and the rate of recovery
29. Prognosis of ARF
• In uncomplicated ARF, such as that due to simple
haemorrhage or drugs, mortality is low even when renal
replacement therapy is required.
• In ARF associated with serious infection and multiple organ
failure, mortality is 50-70%.
• Outcome is usually determined by the severity of the
underlying disorder and other complications, rather than by
renal failure itself.
30. • Serum BUN/creatinine ratio —
• may be greater than 20:1 in prerenal disease due to the
increase in the passive reabsorption of urea that follows the
enhanced proximal transport of sodium and water. Thus, a
high ratio is highly suggestive of prerenal disease.
31. • Urine osmolality —
Loss of concentrating ability is an early and almost universal
finding in ATN with the urine osmolality usually being below
350 mosmol/kg.
In contrast, a urine osmolality above 500 mosmol/kg is highly
suggestive of prerenal disease.
32. urine and serum laboratory values
Prenal Renal
BUN/Cr >20 <20
FeNa <1% >1%
RFI <1% >1%
UNa (mEq/L) <20 > 40
Specific gravity high low
33. acute renal failure: diagnosis
• History and Physical examination
• Blood tests : CBC, BUN/creatinine, electrolytes, uric acid &, CK
• Urine analysis
• Renal Indices
• Renal ultrasound (useful for obstructive forms)
• Doppler (to assess renal blood flow)
34. prerenal ARF:
– Urine sediment: hyaline and fine granular casts
– Urinary to plasma creatinine ratio: high
– Urinary Na: low
– FENa: low
Increased urine output in response to hydration
35. • renal ARF:
– Urine sediment: brown granular casts and tubular epithelial
cells
– Urinary to plasma creatinine ratio: low
– Urinary Na: high
– FENa: high
36. Finding Prerenal ATN
Azotemia
Urine osmolarity >500 <350
(mOsm/kg)
Urine sodium <20 >40
(mmol/d)
Fraction excretion <1 >2
of sodium(%)
Fraction excretion <35 >50
of Urea(%)
Plasma BUN/Cr >20 <10-15
ratio
Urine Cr/Plasma Cr >40 <20
ratio
Urine sediment Bland and/or May show muddy
nonspecific brown granular
casts
37. renal indices
Reabsorption of water and sodium:
- intact in pre-renal failure
- impaired in tubulo-interstitial disease and ATN
Since urinary indices depend on urine sodium concentration, they should be interpreted
cautiously if the patient has received diuretic therapy