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While superficially the language of the health-fraud activists is clearly to do with morally reprehensible phenomena leflunomide 10mg on line medications 4 less, such as charlatanism order 20 mg leflunomide free shipping treatment 5th metatarsal fracture, criminal behaviour and quackery order leflunomide 10 mg medicine x xtreme pastillas, the meta-language often relates to science and its predominant power within the belief system of advanced societies buy generic leflunomide 10mg online symptoms upper respiratory infection. He knew that some would find his book challenging; he had no idea that a handful of people would try to have it banned. Adams did not get a debate; rather, he ran straight into a personal attack which for a short period damaged his professional reputation as a writer and journalist. It was as if a small group of conservative-minded academics and scientists had adopted the strategies of the prewar racetrack gangs. After suggesting the public debate to Jad Adams, Duncan Campbell had vacillated about who should speak first. His presentation, though, was not in the style of a debate; it was a hectoring harangue, for the most part personal rather than scientific or academic. Campbell supported his declamations by saying that more than 18,000 papers had been published in the scientific literature, charting the mechanics of infection and the mechanics of disease spread. If they fail to restore your health, doctors, with their priest-like understanding of life and death, can counsel you during dying. Patients are all only as children, powerless to understand the inner workings of our being. Implicit in this view is the mindless suspension of all critical faculties when considering the historical role of medical science and the peculiarly naive, even ignorant, social, psychological and spiritual views of its practitioners. He did not address the surrounding arguments in the book which placed this theme in context. He attacked the book, not on the grounds that the arguments could be wrong and might be open to debate, but on the grounds that it had been badly written by a stupid person. Every key scientific statement in it is wrong, and provably wrong, and discoverably wrong. Campbell himself, in his unnecessary refutation, made much of the idea of conspiracy. There are people getting on with the job, and there are to be frank, idiots like 6 Duesberg, getting in the way, with no science to back them up. When it came to describing the damaging effect that the book was going to have, Campbell drew upon the authoritative words of his contacts on the Concorde trials — Dr Weller and Dr Farthing. I make these remarks with great seriousness, and I address them to everyone here, particularly I address them to you Cass Mann [turning and looking at Cass Mann on the front row] because you have taken on, in distributing the Positively Healthy Bulletin, the role of informing people who have to deal with this information. It behoves you, having heard this and hearing what is going to be said in reply, to make sure that you fairly, honestly, factually and accurately, distribute the information which you have gleaned from meetings like this. He seems to make little attempt to understand why people might have views that differ from his own and he combines the certainty of science with an intolerable belief in his own entirely personal concept of righteousness. Once Campbell moved off science into the area of personal behaviour, any vestige of rationality was thrown to the wind. In his defence of the Concorde trials and the heroic work of Concorde doctors, Campbell was to aim far higher than a small parochial victory; he wanted the book withdrawn and pulped. Whatever the purpose of the question, it must have occurred to Campbell then, that the opposition which he was both creating and defining was not just going to lie down and play dead. He wrote a damning attack on Jad Adams and his book, both in the New Statesman and the New Scientist, and circulated these prior to their publication to other magazines and journals such as Nature. In retrospect it is clear that Campbell was involved, not simply in a scientific debate, but in a war. It is equally clear that there was more at stake than an opinion, even a fundamental opinion. Regardless of how the rest of the world responded, Campbell careered on after the launch, his balance lost, blurting out threats. In this article, Campbell uses an old propaganda trick: he claimed in the first paragraph that there was a growing campaign against the book, a campaign which he said was having a telling effect. While Campbell began attacks using misleading and outrageous claims, in purple prose, they were presented to Members of Parliament in more conservative and authoritative form in the Digest. Adams did not take legal action against Duncan Campbell, despite the fact that Campbell had woefully misrepresented him. He did, however, contribute an affidavit to the solicitors acting on behalf of the Pink Paper, which at a later date, Campbell was to sue for libel. He also mis-quoted me; put quotation marks around his own paraphrases of my ideas to make it seem I was being quoted and took individual words and phrases out of context so he could place his own, biased, interpretation on them. In the spring of that year, his attention was drawn to two articles by Duncan Campbell, one in the New Statesman and the other in Capital 14 Gay. Deer was informed by contacts that subjects drafted into the Concorde trials were not being given all the information they needed to make an informed choice of treatment. It was a good story about a major drugs trial which was supported by many other referenced stories on other trials, going back beyond the Thalidomide scandal. Deer was the only British journalist who saw clearly, in 1989, that the marketing strategy of Wellcome and Burroughs Wellcome involved tying-up as many available patients as possible. Deer had found out that Ian Weller, one of the central figures in the Concorde trials, working from the Middlesex Hospital and the heroic doctor whom Campbell had written about in 1988, was a Wellcome Fellow. As part of his research, Deer rang Dr Ian Weller, wanting to make last minute checks on his piece. The first was from Martin Sherwood, the public relations manager at the Wellcome Foundation. He wanted desperately to smooth over the situation, to explain everything, to put the matter in another perspective. The second phone call came in the early hours of the next morning, from Duncan Campbell. Campbell accused Deer of having threatened staff at the Academic Department of Genito-urinary Medicine at the Middlesex Hospital where Weller worked. Publicly the conflict between Campbell and Deer surfaced only in a small item in the New Statesman at the end of April. In none of these communications did Duncan Campbell present himself as a socialist in conflict with the right wing press. As far as Andrew Neil was concerned, the conflict which had been thrust upon him, and which involved a journalist renowned for his acerbic personal confrontations, was tangential to the running of a major newspaper. Deer was called in for talks and interviews, and the Sunday Times solicitors were put to work looking for a hook on which to hang an action against Campbell. The campaign which Campbell waged against Deer continued throughout 1989 and early 1990, and ended only when Deer was sent by the Sunday Times to work in America. The War on Cass Mann and Positively Healthy I will decide the route that I will follow. This was the line of enquiry which Brian Deer was to take up with his April articles in the Sunday Times. There was every sign in the first months of 1989 that Positively Healthy would grow in influence. The campaign which Duncan Campbell was planning against Cass Mann, was, however, soon to destroy all the credibility which Positively Healthy had built up.
This could account for low arousal purchase leflunomide from india symptoms 8 days post 5 day transfer, poor fear conditioning generic leflunomide 20 mg otc medications you can take when pregnant, lack of conscience safe 10 mg leflunomide treatment hypothyroidism, and decision-making deficits purchase leflunomide mastercard medications causing hyponatremia. The amygdala is important in aversive conditioning, instrumental learning, 1825 and in responding to emotionally laden facial expressions. Disruptive youths with callous-unemotional traits fail to activate the amygdala when processing fearful expressions. Maternal nutritional deprivation during early pregnancy in wartime Holland has been associated with antisocial personality disorder in young adult offspring. Adoptive parents may show negative parenting when the parents of their children had antisocial proclivities, possibly reacting to some inherited trait in the children. Novelty seeking may be associated with the type 4 dopamine receptor (but this was not so in a meta-analysis: Kluger ea, 2002) and the type 1 cannabinoid receptor. According to Fu ea, (2002) who studied male twin pairs who served in Vietnam, shared risks between antisocial personality disorder, major depression and marijuana dependence may be explicable as stemming from the antisocial personality disorder. It does appear that parenting style can moderate the doing something despite negative consequences, and this tendency is found in animals who have a dysfunctional septo-hippocampal system. The neuronal isoforms of nitric oxide synthase may be involved in modifying various behaviours, including aggression, and deficits in neuronal signalling via nitric oxide in moderating prefrontal circuitry may be important in the origin of impulsiveness. The screening version contains interpersonal/affective (superficial, grandiose, manipulative, lacking remorse, no empathy, doesn’t accept responsibility) and social deviance (impulsive, poor control of behaviour, lacking goals, irresponsible, antisocial as adolescent and adult) factors. Psychopathy is a narrower concept than antisocial personality disorder, insofar as the former may not have broken overt rules or have been caught doing so. The former had impairments on dorsolateral prefrontal cortical executive function tasks of planning ability and set shifting. Antisocial personality disorder is nearly always preceded by conduct disorder (see box) in childhood. A 40 year follow-up of conduct-disordered adolescents (Colman ea, 2009) found that they were likely to leave school without any qualifications and to experience many social and health problems that had adverse effects on them, their families, and society. Children who have early feeding, washing, or dressing problems, who cry loudly, who protest at novelty, and who have tantrums may later be over-represented among the ranks of psychopathy. The earlier the onset of conduct disorder in childhood and the more pervasive it is the more likely is antisocial personality disorder to be present in adulthood. Also, environmental deprivation is more closely linked to antisocial behaviour than is social class. Some findings 1831 suggest a dysregulation of the hypothalamico-pituitary-adrenal axis in conduct disorder and antisocial personality disorder. Conduct disorder Not an entity in itself Various forms of unacceptable behaviour Different levels of severity Prevalence: 1% - 10% M > F, but females may be catching up1832 Reading disorder in one-third Family (e. Childhood adversity associated with maladaptive family functioning is a strong predictor of chronic functional impairment. The outlook tends towards improved social behaviour with time (Paris, 2002) but there remains the possibility of domestic violence thereafter. Problems, ranging from illness to early demise, may result from accidents, drug and alcohol abuse, fighting etc. Many, if not the majority, of psychiatrists, hold that there is no legitimate treatment for personality disorder in general and psychopathic personality disorder in general. There is persistent defiance toward authority (teachers and other adults) characterised by hostility, resentment, and argumentativeness. The syndrome is more common in young boys than young girls but it affects the sexes equally by adolescence. Symptoms are more often displayed in front of people familiar to the child and may not be revealed to the clinician. Early onset, aggression, poverty, and parental drug abuse favour the development of conduct disorder. Female adolescent conduct disorder may progress to antisocial personality disorder and somatoform disorder, depression and other ‘internalizing’ conditions. Social problems, especially deviant peers, are significant factors in the genesis of adolescent-onset cases, i. The author is aware of inner urban dwellers who had no moral qualms about stealing from ‘outsiders’ but who were outraged if one of their peers stole from a neighbour! This may be a product of ‘outsiders’ being seen as ‘haves’ and the subculture/neighbourhood as ‘have not’s. There is affective instability, minimal planning and frequent angry outbursts, with violent and explosive behaviour. Borderlines recall less parental care than do non-borderlines, especially from the mothers. They are lonely, lacking in emotional tone, anhedonic, and have a low stress tolerance. Regression and transient psychosis often occur during psychotherapy – thoughtless attempts to ‘probe the emotional depths’ of these patients may exacerbate the situation. This fact and complications may account for suggested relationships with schizophrenia and affective disorders. Torgersen ea, 2001) Perhaps females are more likely to look for or be referred for treatment. Pope ea (1985) diagnosed ‘factitious psychosis’ in two of their cases, both of whom also had factitious neurological symptoms. The term factitious is problematic in such cases because it has been variably defined as ‘subconscious’ or ‘simply seeking (inappropriate) medical care’. Psychosis in borderline personality disorder may be associated with drugs or mood disorder. Lynch (2008) discussed Linehan’s ‘biosocial’ theory in relation to borderlines: emotional vulnerability (high sensitivity and reactivity and slow return to baseline), environmental invalidation (being told that one is wrong – this is associated with autonomic hyperactivity as shown by the galvanic skin response) and problems with regulating emotions interact. The person is hyperresponsive to environmental cues/triggers that lead to emotional dysregulation (Fertuck ea  found that borderlines have an enhanced sensitivity to the mental states of others. Therapists need a ‘consultation team’ to call on for support because patients may dysregulate the therapist. Borderlines are better than controls at assessing facial expressions for all emotions. Treatment aims to prevent the self-cutting response and replace it with problem-solving. Finally, when separation threatens, psychic decompensation follows with increasing levels of harm to the self. Stevenson ea, 2005) Drugs are also used although the risk of abuse is increased; some authors eschew treatment of ‘secondary’ problems like mood problems or ‘voices’, suggesting that they improve once control over impulsiveness and anger is achieved. In the present author’s experience, a patient may appear to be doing very well between psychotherapy sessions and suddenly kill themselves because of an event outside the therapist’s control, e. There are moments during treatment when sense of self is disrupted by traumatic memories. Therapist empathy with the patient and reflections help the patient to think about and gain understanding of what is happening within the self and between therapist/others and the self (mentalisation or reflective function). According to Bateman & Fonagy (2008, 2009) mentalisation therapy has long-term beneficial effects, although Choi-Kain and Gunderson (2008), who see mentalisation as excessively broad and multi- faceted, are sceptical. Zanarini (2005a) has presented follow-up evidence suggesting that both symptomatic remission and attainment of good psychosocial functioning are common among even very disturbed cases, remarking that they ‘get well, as if they are growing up out of this disorder’.
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Chylomicrons therefore function to: • deliver dietary triacylglycerols to adipose tissue and muscle • deliver dietary cholesterol to the liver purchase leflunomide with mastercard symptoms checker. The endocytosed membrane vesicles (endosomes) fuse with lysosomes cheap 10mg leflunomide overnight delivery medications zoloft side effects, in which the apoproteins are degraded and the cholesterol esters are hydrolysed to yield free cholesterol purchase leflunomide us treatment type 2 diabetes. The precise mechanism for these effects is unclear leflunomide 20mg visa medications herpes, but it may be mediated through the regulation of apo-B degradation. This process has the effect of lowering the level of intracellular cholesterol, since the cholesterol stored within cells as cholesteryl esters will be mobilised to replace the cholesterol removed from the plasma membrane. Lysosomal enzymes degrade the apoproteins and release free fatty acids and cholesterol. This can lead to excess circulating levels of cholesterol and cholesteryl esters when the dietary intake of fat and cholesterol is excessive. Excess cholesterol tends to be deposited in the skin and tendons and within the arteries, which can lead to atherosclerosis. Individuals suffering from diabetes mellitus, hypothyroidism or kidney disease often exhibit abnormal lipoprotein metabolism as a result of secondary effects of their disorders. The resultant hypercholesterolaemia leads to premature coronary artery disease and atherosclerotic plaque formation. Familial hypercholesterolaemia was the ﬁrst inherited disorder recognised as being a cause of myocardial infarction (heart attack). Caucasians and Japanese with the apo-E-ε4 isoform have between 10 and 30 times the risk of developing Alzheimer’s by 75 years of age. While the exact mechanism is unknown, evidence suggests an interaction with amyloid. Alzheimer’s disease is characterised by plaques consisting of the peptide beta-amyloid. However, the isoform apo-E-ε4 is much less effective, which might result in an increased vulnerability to Alzheimer’s in individuals with that gene variation. Drug therapy is considered as an option only if non-pharmacologic interventions (altered diet and exercise) have failed to lower plasma lipids. These are compounds that bind bile acids; the drop in hepatic reabsorption of bile acids releases a feedback inhibition, resulting in a greater amount of cholesterol being converted to bile acids to maintain a steady level in the circulation. Focus on: atherosclerosis ‘Arteriosclerosis’ is a general term describing any hardening or loss of elasticity of medium or large arteries, and refers to the formation of an atheromatous plaque. Lipoprotein-associated phospholipase A2 is an emerging cardiovascular risk marker. Monocytes enter the artery wall from the bloodstream, with platelets adhering to the area of insult. This membrane protein mediates leukocyte-endothelial cell adhesion and signal transduction, and may play a role in the development of atherosclerosis and rheumatoid arthritis. There is also smooth- muscle proliferation and migration from tunica media to intima, responding to cytokines secreted by damaged endothelial cells. They are thought to participate in the removal of many foreign substances and waste materials in the body. It is characterised by a remodelling of arteries involving the concomitant accumulation of fatty substances called plaques. As the plaques grow, artery wall thickening occurs without any narrowing of the artery lumen; stenosis, the narrowing of the artery opening, is a late event, which may or may not occur, and is likely the result of repeated plaque rupture and healing responses. Most commonly a plaque will rupture, forming a thrombus, which can rapidly slow or stop blood ﬂow, leading to death of the tissues fed by the artery: an infarction. There is some evidence that atherosclerosis may be caused by an infection of the vascular smooth-muscle cells. Chickens, for example, develop atherosclerosis when infected with the Marek’s disease herpesvirus. Herpesvirus infection of arterial smooth-muscle cells has been shown to cause cholesteryl ester accumulation, which is associated with atherosclerosis. Various anatomical, physiological and behavioural risk factors for atherosclerosis are known. Many of these are recognised within the ‘metabolic syndrome’, a combination of disorders that increases the risk of developing cardiovascular disease and diabetes. Rosuvastatin is a statin shown to demonstrate regression of atherosclerotic plaque within the coronary arteries. The antioxidant effects of the statins may be partly responsible for their therapeutic success. Two main liver lobes are each made up of thousands of lobules; lobules connect to small ducts that connect to larger ducts, forming the hepatic duct. The hepatic duct transports bile, produced by the hepatocytes, to the gallbladder and duodenum. The liver regulates, synthesises, stores and secretes many important proteins and nutrients, and puriﬁes, transforms and clears toxic or unnecessary compounds from the blood. Hepatocytes are optimised for function through their contact with sinusoids (leading to and from blood vessels) and bile ducts. A special feature of the liver is its ability to regenerate, maintaining function even in the face of moderate damage. In utero, energy is provided by glucose, with liver metabolism being directed to glucose degradation; activity of the rate-limiting enzymes of glycolysis, hexokinase and phospho- fructokinase is high. With the onset of post-natal life, and an intake of a fat-rich and carbohydrate-poor diet, infants develop the ability to synthesise glucose de novo from non-carbohydrate precursors (gluconeogenesis). In the inherited condition of Wilson’s disease, the secretion of copper into bile is abnormal, resulting in a low blood level of the copper-binding protein ceruloplasmin. Glycogen is mainly stored in the liver and muscle cells, but the kidneys and intestines also store some limited amounts of glycogen (Table 6. The inability to degrade glycogen may cause cells to become pathologically engorged, lead- ing to a functional loss of glycogen as an energy source and a blood glucose buffer. For example, the enzyme glucose-6-phosphatase is localised on the cisternal (inner) surface of the endoplasmic reticulum, and glucose-6-phosphate must be transported (translocated) across the endoplasmic reticulum to gain access to the enzyme. Mutation of either the phosphatase or the translocase will lead to symptoms characteristic of von Gierke’s disease. Hepatocytes secrete bile into canaliculi, then into bile ducts, where it is modiﬁed by addition of a bicarbonate-rich secretion from ductal epithelial cells. Further modiﬁcation occurs in the gall bladder, where it is concentrated up to ﬁvefold, through absorption of water and electrolytes. Only relatively small quantities of bile acids are lost from the body; approximately 95% of bile acids delivered to the duodenum are absorbed back into blood within the ileum. Venous blood from the ileum goes straight into the portal vein, and hence through the sinusoids of the liver (enterohepatic circulation). Hepatocytes extract bile acids very efﬁciently from sinusoidal blood; they are re-secreted into canaliculi. The net result of enterohepatic recirculation is that each bile salt molecule may be reused up to 20 times, and often 2 or 3 times during a single digestive phase (Figure 6. Liver disease, and damage to the canalicular system, can result in escape of bile acids into the systemic circulation. Assay of systemic levels of bile acids is used clinically as a sensitive indicator of hepatic disease.
This is the most comfortable position and allows free gravitational drainage of the pelvis and easy observation of any tendency for the kidneys to descend best order for leflunomide treatment 4 hiv. In children generic 10 mg leflunomide with visa medicine cups, the study is performed more easily if the patient is lying in the supine position on the couch discount leflunomide 20mg overnight delivery medications like prozac. An image of the pelvis and bladder before and after micturition and/or after five minutes in the upright position to ensure gravita- tional drainage is recommended in the event of pelvic retention at the end of the study order leflunomide online now treatment atrial fibrillation. The injection should be less than 1 mL in volume and either given rapidly or pushed by a bolus of saline through a three way stopcock. The injection should be given in one single continuous movement of the syringe plunger. The use of frame times greater than 15 s reduces the temporal resolution of the study so that the sharpness of the peak of the renogram and the quality of the analysis can be impaired. Interpretation A holistic approach to interpretation should be made combining images, renograms, numerical results and interventions (see below). A report should contain the demographic data, the name of the test, type and activity of the injected radiopharmaceutical, any interventions and any patient reactions (e. It should also include a description of the images and curves, the numerical data, a separate conclusion and a separate recommendation or clinical advice when appropriate. A description of the images should consider relative renal size, cortical or parenchymal defects and retention of activity in the parenchyma or pelvis. Unusual anatomy features such as an ectopic, duplex or horseshoe kidney should be recorded. Normal renogram curves are symmetric in shape and height, and three phases can be identified: an uptake phase with rapid upslope, a parenchymal transit phase with less pronounced upslope ending in a peak of maximum activity, and an excretion phase. The background subtracted renograms should be described in terms of: —The characteristics of the uptake and parenchymal phases; —The presence and sharpness of the peaks; —Whether the peaks occur at the same time (time to maximum activity); —The shape of the third phases, or the continuing rise of the curve with no excretion phase. The relative function considering the normal range of 43–57% for each kidney should be noted. If there is a duplex kidney, the relative function of the upper and lower portions should also be given. There are various measurements that can be made from the time–activity curve to characterize its shape, typically ratios of one point on the second phase or peak activity time and one point on the third phase. These may be helpful in straightforward cases but give disappointing results when renal function is poor or in more complex cases. Besides relative function, there are other physiological measurements that can be done. Firstly, there are the times for the tracer to reach the nephrons, cortex and pelvis. The value is given as a percentage for a specified time, usually 30 min, and has the merit of being independent of the level of renal function. Outflow efficiency is calculated as the percentage of the activity entering the kidney that is discharged in 30 min. Correction of this disorder in one kidney leads to a normalization of blood pressure, provided the other kidney is functioning normally. Renovascular disorders may be symmetrical when caused by systemic pathology such as glomerulonephritis, diabetes, autoimmune diseases and accelerated hypertension. It may be asymmetrical when caused by small vessel disease such as in pyelonephritis, tuberculosis, endarteritis, amyloid or renal vein thrombosis and large vessel disease, for example unilateral or bilateral renal artery stenosis or fibromuscular hyperplasia, or in association with a resistance to outflow. The features of renovascular disorder are a reduced relative function, an impaired second phase of the renogram, a delayed peak of over 60 s compared with the contralateral kidney and a prolonged mean parenchymal transit time of over 240 s. There is no action on the afferent arterioles, which are maximally dilated through autoregulation in response to the renovascular disorder. Blood pressure is monitored before and at 5 min intervals after the oral administration of Captopril. If the diastolic pressure falls by 10 mmHg or more during the subsequent hour, this is an indication that Captopril has been absorbed and the test may be started. It is sometimes recommended that the patient fasts for at least four hours before the Captopril test, during which time a normal amount of fluid is given to assure hydration. Infusion of saline during the study is not necessary unless it is known or suspected that the patient is salt depleted, in which case a severe hypotensive response may be observed. Interpretation The images may show parenchymal retention of activity at the side of the renovascular disorder, persisting longer after use of Captopril compared with a baseline study because the absence of filtration fluid precludes washout of the tubulary secreted agents. Numerical indices such as the corticopelvic transfer time (measuring the time of first appearance of activity in the kidneys and the first appearance of activity in the pelvis) may be recorded and compared between baseline and Captopril values. The time–activity curve should deteriorate in shape in comparison with the baseline; in particular there should be impairment of the second phase, further prolongation of the peak time and deterioration or absence of the third phase. If unilateral renovascular disorder is suspected, the contralateral kidney should show a normal renogram and indices. It should be recognized that renal artery stenosis, common in the elderly as a result of atheroma, might co-exist with essential hypertension, which is also very common in this population. This does not mean that renal artery narrowing, as seen on renal artery angiography, is the cause of renovascular disorder or hypertension. Only renal radionuclide studies can distinguish whether narrowing of a renal artery is functionally significant. This may be due to small vessel disease although additional large vessel disease can be present. When the response to Captopril is symmetrical, small vessel disease is most likely. Principle Furosemide is a potent diuretic which inhibits the reabsorption of salt and secondary water in the ascending limb of the loop of Henle. Its diuretic action is dependent on the level of renal function, particularly the number of nephrons in the kidney, the absence of both sodium and chloride depletion, and the absence of hypotension. Definitions Dilatation of the collecting system does not necessarily mean obstruction. Absence of dilatation does not exclude obstruction, particularly in an oliguric patient. The following definitions may be helpful: (a) Obstructing uropathy is a change in the outflow tract due to an obstructing process. There is still fluid flowing down the ureter in the presence of a chronically increased resistance to outflow. Firstly, the intratubular luminal pressure is marginally greater (fractions of a millimetre of water) 240 5. Secondly, the resistance also causes a reduction in the amount of excreted activity compared with the amount that has been initially taken up. The consequence of these processes is that the third phase of the time–activity curve fails to fall as rapidly as expected or may even continue to rise. Clinical indications Clinical indications for diuretic renography are: (a) Suspected obstructive nephropathy or obstructing uropathy associated with hydronephrosis or renal stones, malignancy or retroperitoneal fibrosis, etc. Procedure The procedure should be explained to the patient and, in the case of a child, to the parents or carers.