Acute (sudden) kidney failure is the sudden loss of the ability of the kidneys to remove waste and concentrate urine without losing electrolytes.
Symptoms
• Anorexia.
• Bloody stools.
• Breath odor.
• Brusing easily.
• Changes in mental status or mood.
• Decreased appetite.
• Decreased sensation, especially in the hands or feet.
• Dyspnoea.
• Fatigue.
• Flank pain (between the ribs and hips).
• Haematuria.
• Hand tremor.
• Headache.
• High blood pressure.
• Lethargy.
• Metallic taste in mouth.
• Nausea or vomiting may last for days.
• Nosebleeds.
• Palpitation.
• Persistent hiccoughs.
• Prolonged bleeding.
• Seizures gait.
• Slow, sluggish movements.
• Swelling – generalized (fluid retention).
• Swelling of the ankle, feet, and leg swelling.
• Urination changes:
o Decrease in amount of urine.
o Excessive urination at night.
o Urination stops completely.
Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss of renal function over a period of months or years. The symptoms of worsening kidney function are unspecific, and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic kidney disease may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia or pericarditis.
Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a falling glomerular filtration rate (rate at which the kidneys filter blood) and as a result a decreased capability of the kidneys to excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis (testing of a urine sample) shows that the kidney is allowing the loss of protein or red blood cells into the urine. To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests and often renal biopsy (removing a small sample of kidney tissue) are employed to find out if there is a reversible cause for the kidney malfunction.
Recent professional guidelines classify the severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is also called established chronic kidney disease and is synonymous with the now outdated terms end-stage renal disease (ESRD), chronic kidney failure (CKF) or chronic renal failure (CRF).
Symptoms
• Fatigue
• Frequent hiccups
• General ill feeling
• Generalized itching (pruritus)
• Headache
• Nausea, vomiting
• Unintentional weight loss.
• Anorexia.
• Polyuria.
• Nocturia.
• Swelling of face.
Acute glomerulonephritis (AGN) is active inflammation in the glomeruli. Each kidney is composed of about 1 million microscopic filtering “screens” known as glomeruli that selectively remove uremic waste products. The inflammatory process usually begins with an infection or injury (e.g., burn, trauma), then the protective immune system fights off the infection, scar tissue forms, and the process is complete.
There are many diseases that cause an active inflammation within the glomeruli. Some of these diseases are systemic (i.e., other parts of the body are involved at the same time) and some occur solely in the glomeruli. When there is active inflammation within the kidney, scar tissue may replace normal, functional kidney tissue and cause irreversible renal impairment.
The severity and extent of glomerular damage—focal (confined) or diffuse (widespread)—determines how the disease is manifested. Glomerular damage can appear as subacute renal failure, progressive chronic renal failure (CRF); or simply a urinary abnormality such as hematuria (blood in the urine) or proteinuria (excess protein in the urine).
Etiology
An immunological disorder.
History of
Streptococcal throat or skin infection.
Scabies with impetigo.
Mealsles.
Age
Common in children.
Sex
Equal incidence.
CLINICAL FEATURES
Symptoms
Onset: sudden.
Swelling of face in morning.
Gradually swelling of whole body.
Oliguria.
Haematuria.
Low grade fever.
Headache.
Weakness.
Anorexia.
Nausea, vomiting.
Constipation.
Dyspnoea.
Signs
Temperature: 38-38.5C.
Pulse: fast.
Blood pressure: raised.
Face: puffy.
Oedema: pitting.
Renal angle: may be tender.
Tonsils: enlarged, congested.
Heart: apex out, forceful.
Complication
Acute renal failure.
Hypertensive left ventricular failure.
Hypertensive encephalopathy.
Secondary infection.
General Management
Bed rest till haematuria, hypertension, fever, edema, ESR, subside.
Diet
Protein restriction.
Salt restriction.
Fluid restriction according to urinary output.
Diet consisting of glucose, barely water, rice, potatoes should be encouraged.
.Renal calculi can vary in size from as small as grains of sand to as large as a golf ball.Location and quality of pain are related to position of the stone within the urinary tract. Severity of pain is related to the degree of obstruction, presence of ureteral spasm, and presence of any associated infection.
Etiology/Cause
HYPEREXCRETION OF RELATIVELY INSOLUBLE URINARY CONSTITUENTS such as oxalates, calcium, uric acid, cystine and certain drugs (such as magnesium trisilicate in the treatment of peptic ulcer).
PHYSIOLOGICAL CHANGES IN URINE such as Urinary pH (which is influenced by diet and medicines), Colloid content, Decreased concentration of crystalloids, Urinary magnesium/calcium ratio.
ALTERED URINARY CRYSTALLOIDS AND COLLOIDS.
0. Either there is an increase in the crystalloid level or a fall in the colloid level, urinary stones may be formed.
0. If there is any modification of the colloids e. g. they lose their solvent action or adhesive property, urinary stones may develop.
DECREASED URINARY OUTPUT OF CITRATE.
VITAMIN A DEFICIENCY.
The desquamated cells form nidus for stone formation. This is more applicable to bladder stones.
• URINARY INFECTION.
• URINARY STASIS.
• HYPERPARATHYROIDISM.
3. Due to overproduction of parathormone the bones become decalcified and calcium concentration in the urine is increased. This extra calcium may be deposited in the renal tubules or in the pelvis to form renal calculus.
• PROLONGED IMMOBILISATION.
PREDISPOSING FACTORS
ENVIRONMENTAL AND DIETARY FACTORS
• Low urine volumes.
• High ambient temperatures.
• Low fluid intake.
• Diet.
• High protein intake.
• High sodium.
• Low calcium.
• High sodium excretion.
• High oxalate excretion.
• High urate excretion.
• Low citrate excretion.
CONGENITAL AND INHERITED CONDITIONS
• Familial hypercalciuria
• Medullary sponge kidney
• Cystinuria
• Renal tubular acidosis type I
• Primary hyperoxaluria
Symptoms
• Colicky pain: “loin to groin”. Often described as “the worst pain […] ever experienced”.
• Hematuria: blood in the urine, due to minor damage to inside wall of kidney, ureter and/or urethra.
• Pyuria: pus (white blood cells) in the urine.
• Dysuria: burning on urination when passing stones (rare). More typical of infection.
• Oliguria: reduced urinary volume caused by obstruction of the bladder or urethra by stone, or extremely rarely, simultaneous obstruction of both ureters by a stone.
• Abdominal distension.
• Nausea/vomiting: embryological link with intestine – stimulates the vomiting center.
• Fever and chills.
• Hydronephrosis.
• Postrenal azotemia: when kidney stone blocks ureter.
• frequency in micturation: Defined as an increase in number of voids per day (>than 5 times), but not an increase of total urine output per day (2500 ml). That would be called polyuria.
• loss of appetite.
• loss of weight.
INVESTIGATIONS
• Blood examination.
• Urinalysis.
• Radiography.
. Straight X-ray.
. Excretory urogram.
• Ultrasonography.
• Computed tomography.
• Renal Scan.
• Cystoscopy.
• Stone analysis.
The following investigations are appropriate in bilateral and recurrent stone formers:
• Serum calcium, measured fasting on three occasions to exclude hyperparathyroidism
• Serum uric acid
General management
The general measures or advises which should be given to the patient regardless of the type of stone are:
• Fluid intake should he high at all times. Fluids should be taken at bed time so that nocturia will occur. This will prevent dehydration.
• Avoidance of milk, cheese and great deal of calcium should be advised. If renal function is satisfactory, sodium cellulose phosphate 5 g T.D.S. with meals should be prescribed to reduce calcium absorption.
• Urine should be kept acid all the time. Alkalies should be prohibited or used in lesser quantities in those patients who are suffering from peptic ulcer.
• Vitamin D should be stopped or used in very low quantity.
• Patients with hyperuricemia should avoid red meats, offal and fish, which are rich in purines, and should receive treatment with allopurinol.
• Eggs, meat and fish are high in sulphur containing proteins and should be restricted in patients with cystinuria.
Nephrotic syndrome is a set of signs or symptoms that may point to kidney problems. The kidneys are two bean-shaped organs found in the lower back. Each is about the size of a fist. They clean the blood by filtering out excess water and salt and waste products from food. Healthy kidneys keep protein in the blood, which helps the blood soak up water from tissues. But kidneys with damaged filters may leak protein into the urine. As a result, not enough protein is left in the blood to soak up the water. The water then moves from the blood into body tissues and causes swelling.
Kidneys affected by nephrotic syndrome have small pores in the podocytes, large enough to permit proteinuria (and subsequently hypoalbuminemia, because some of the protein albumin has gone from the blood to the urine) but not large enough to allow cells through (hence no hematuria). By contrast, in nephritic syndrome, RBCs pass through the pores, causing hematuria.
Childhood nephrotic syndrome can occur at any age but is most common between the ages of 1½ and 5 years. It seems to affect boys more often than girls.
ETIOLOGY
• IDIOPATHIC
• RENAL DISEASE
1. Minimal glomerulonephritis (common in children).
2. Membranous glomerulonephritis (common in adults).
• IATROGENIC
1. NSAID’s.
2. Gold.
3. Bismuth.
4. D-Penicillamine.
• ALLERGY
1. Bee sting.
2. Serum sickness.
• INFECTIONS
1. Malaria.
2. Sub-acute bacterial endocarditis.
• METABOLIC
1. Diabetes mellitus.
• SYSTEMIC DISEASES
1. S.L.E.
2. Amyloidosis.
• MALIGNANCY
1. Lymphoma.
2. Leukaemia.
3. Multiple myeloma.
CLINICAL FEATURES
Symptoms
• Onset: insidious.
• Swelling of face, spreading to whole body.
• Oliguria.
• Dyspnoea.
• Anorexia.
• Nausea, vomiting.
• Lethargy, tiredness.
• Susceptibility to infections.
Signs
• Nephritic facies
o Puffy face.
o Baggy eyelids.
o Waxy pallor.
• Anaemia: mild to moderate.
• Oedema: pitting.
• Pulse: fast.
• Blood pressure: normal or low.
• Abdomen:
o Bloated.
o Flanks full.
o Skin shiny.
o Fluid thrill / shifting dullness present.
• Chest:
o Signs of bilateral hydrothorax may be present.
Complications
• Venous thrombosis: due to leak of anti-thrombin 3, which helps prevent thrombosis. This often occurs in the renal veins. Treatment is with oral anticoagulants (not heparin as heparin acts via anti-thrombin 3 which is lost in the proteinuria so it will be ineffective.)
• Infection: due to leakage of immunoglobulins, encapsulated bacteria such as Haemophilus influenzae and Streptococcus pneumonia can cause infection.
• Acute renal failure is due to hypovolemia. Despite the excess of fluid in the tissues, there is less fluid in the vasculature. Decreased blood flow to the kidneys causes them to shutdown. Thus it is a tricky task to get rid of excess fluid in the body while maintaining circulatory euvolemia.
• Pulmonary edema: again due to fluid leak, sometimes it leaks into lungs causing hypoxia and dyspnoea.
• Growth retardation: does not occur in MCNS.It occurs in cases of relapses or resistance to therapy. Causes of growth retardation are protein deficiency from the loss of protein in urine, anorexia (reduced protein intake), and steroid therapy (catabolism).
• Vitamin D deficiency can occur. Thyroxine is reduced due to decreased thyroid binding globulin.
• Microcytic hypochromic anaemia is typical. It is iron-therapy resistant.
GENERAL MANAGEMENT
• Bed rest, if severe oedema or infection is present.
• High protien diet: 1.5-3 g / kg.body weight (if blood urea is normal).
• Salt restriction.
• Fluid restriction according to urinary output
Polycystic kidney disease (PKD) is a genetic disorder characterized by the growth of numerous cysts in the kidneys. The kidneys are two organs, each about the size of a fist, located in the upper part of a person’s abdomen, toward the back. The kidneys filter wastes and extra fluid from the blood to form urine. They also regulate amounts of certain vital substances in the body. When cysts form in the kidneys, they are filled with fluid. PKD cysts can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure.
When PKD causes kidneys to fail—which usually happens after many years—the patient requires dialysis or kidney transplantation. About one-half of people with the most common type of PKD progress to kidney failure, also called end-stage renal disease (ESRD).
PKD can also cause cysts in the liver and problems in other organs, such as blood vessels in the brain and heart. The number of cysts as well as the complications they cause help doctors distinguish PKD from the usually harmless “simple” cysts that often form in the kidneys in later years of life.
Etiology
Genetic disorder.
Inheritance: autosomal dominant.
Types
• Autosomal dominant PKD is the most common, inherited form. Symptoms usually develop between the ages of 30 and 40, but they can begin earlier, even in childhood. About 90 percent of all PKD cases are autosomal dominant PKD.
Autosomal recessive PKD is a rare, inherited form. Symptoms of autosomal recessive PKD begin in the earliest months of life, even in the womb.
Acquired cystic kidney disease (ACKD) develops in association with long-term kidney problems, especially in patients who have kidney failure and who have been on dialysis for a long time. Therefore, it tends to occur in later years of life. It is not an inherited form of PKD.
CLINICAL FEATURES
Symptoms
Dull aching in loins.
Vague abdominal pain.
Frequent urination.
Haematuria.
Headache.
Drowsiness.
Anorexia.
Signs
Anaemia: moderate to severe.
Blood pressure: raised.
On palpation abdomen
Enlarged irregular kidneys.
Large knobby renal masses.
Enlarged polycystic liver (50% cases).
COMPLICATIONS
• Recurrent urinary tract infection.
• Renal calculi.
• Chronic renal failure.
GENERAL MANAGEMENT
Control of blood pressure.
Plenty of fluids.
Low protein diet.
Correction of anaemia (due to haematuria).
Prevention & prompt treatment of infection.
UTIs are most common in sexually active women and increase in diabetics and people with sickle-cell disease or anatomical malformations of the urinary tract.
Since bacteria can enter the urinary tract through the urethra (an ascending infection), poor toilet habits can predispose to infection, but other factors (pregnancy in women, prostate enlargement in men) are also important and in many cases the initiating event is unclear.
A urinary tract infection, or UTI, is an infection that can happen anywhere along the urinary tract. The urinary tract includes the:
Bladder.
Kidneys.
Ureters – the tubes that take urine from each kidney to the bladder.
Urethra – the tube that empties urine from the bladder to the outside.
Etiology
ACUTE U.T.I.
Causative organism
E. coli.
Staphylococci.
Klebsiella.
Candida.
Proteus.
Entrococci.
Predisposing causes
Female sex.
Enlarged prostate.
Neuropathic bladder.
Urinary tract calculi.
Polycystic kidney disease.
Diabetes mellitus.
Vesico-ureteric reflex.
Bladder catheterisation.
CHRONIC U.T.I.
Mal-treated acute U.T.I.
Urinary obstruction
Enlarged prostate.
Stricture.
Stone.
Stasis in bladder
Cystocele.
Neurogenic bladder.
Vesico-ureteric reflux.
Polycystic kidney disease.
Diabetes mellitus.
Symptoms
For bladder infections
Frequent urination along with the feeling of having to urinate even though there may be very little urine to pass.
Nocturia: Need to urinate during the night.
Urethritis: Discomfort or pain at the urethral meatus or a burning sensation throughout the urethra with urination (dysuria).
Pain in the midline suprapubic region.
Pyuria: Pus in the urine or discharge from the urethra.
Hematuria: Blood in urine.
Pyrexia: Mild fever
Cloudy and foul-smelling urine
Increased confusion and associated falls are common presentations to Emergency Departments for elderly patients with UTI.
Some urinary tract infections are asymptomatic.
Protein found in the urine. Cloudy urine
Foul or strong urine odor
Frequent or urgent need to urinate
Low fever (not everyone will have a fever)
Need to urinate at night
Pain or burning with urination
Painful sexual intercourse
Pressure in the lower pelvis
For kidney infections
All of the above symptoms.
Emesis Vomiting is common.
Back, side (flank) or groin pain.
Abdominal pain or pressure.
Shaking chills and high spiking fever.
Night sweats.
Extreme fatigue. Chills and shaking
Fatigue
Fever above 102 degrees Fahrenheit, which lasts for more than 2 days
Flank (side) pain
Flushed, warm, or reddened skin
General ill feeling
Mental changes or confusion (in the elderly, these symptoms often are the only signs of an UTI)
Nausea and vomiting
Severe abdominal pain (sometimes)
PREVENTION
Drink plenty of liquids to flush bacteria out of the urinary system.
Wipe from the vagina to the anus after defecation to avoid spreading bacteria.
Drink water before and after sex so that one will urinate a good volume with a steady stream afterwards. This will help eliminate any bacteria that may have entered.
Consider using another method of birth control or a different brand of condom for your spouse if you suspect that chemical over the condom is causing irritation.
Avoid tight clothing. It may irritate tissues, trap heat, and promote bacterial growth.
Wear cotton underwear. Cotton is less irritating and provides more ventilation than nylon.
Complication
Renal calculi.
Hypertension.
Chronic renal failure.
GENERAL MANAGEMENT
Bed rest.
Plenty of fluids.
Regular voiding of urine.
Maintain alkalinity of urine.
Local hygiene.
Salt restriction, if blood pressure is high.
Protein restriction, if blood urea is high.