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This information had to form part of a programme that educated them about the disease zenegra 100mg visa. Older people do not always learn easily from information given on paper and some people may need psychological support to help them cope with the consequences of the information that they have been given order zenegra 100mg line. We do not believe this recommendation will have a big cost impact for the NHS since this is part of the existing National Service Framework and such programmes are already widespread buy zenegra 100 mg without a prescription. R71 When developing information or education programmes, involve people with CKD in their development from the outset. The following topics are suggested: q What is CKD and how does it affect people? R72 Offer people with CKD high quality information or education programmes at appropriate stages of their condition to allow time for them to fully understand and make informed choices about their treatment R73 Healthcare professionals providing information and education programmes should ensure they have specialist knowledge about CKD and the necessary skills to facilitate learning. R74 Healthcare professionals working with people with CKD should take account of the psychological aspects of coping with the condition and offer access to appropriate support (for example, support groups, counselling or a specialist nurse). A number of tools have recently been introduced to help identify people with CKD and aid early intervention and appropriate management to reduce/prevent complications and progression of CKD. In March 2006 guidelines for the identification, management and referral of adult patients with chronic kidney disease were published by the Royal College of Physicians of London on behalf of a number of collaborating agencies. Participation by practices in the QOF is voluntary, but participation rates are high possibly because there is a financial incentive to do this. In March 2006, four renal domains were included for the first time in the QOF. These indicators focused on creating a register of people with chronic kidney disease with an eGFR <60 ml/min/1. These national tools have increased referral of people with CKD to their local specialist and in turn have resulted in a number of local initiatives aimed at providing a structured delivery of care for people with kidney disease in partnership with primary care. This section was aimed at identifying whether any of these tools had yet improved the identification and management of adults with CKD. Outcomes of interest were appropriate investigations and follow-up, referral, medicines management, and achieving clinical targets. The New Opportunities for Early Renal Intervention by Computerised Assessment (NEOERICA) project used computer searching to extract a retrospective dataset of all patients with a valid serum creatinine measurement from 17 primary care practices in the UK (N=38,262 with valid serum creatinine measures). Manual searching 182 15 Information needs of medical records from 1 practice (N=492 with stages 3–5 CKD identified by computer searching) was used to test the validity of computer searching to estimate the prevalence of CKD. Serum creatinine measurements were calibrated to the original MDRD study in Stevens et al. Two publications from the Optimal Renal Care UK (ORC UK) study assessed the utility of a disease management programme (DMP) that was guideline- and algorithm-based to identify, manage, and appropriately refer people with CKD. Medications dispensed prior to the index creatinine measurements were used to determine disease categories, which were considered in a stepwise logistic regression analysis. Risk scores were calculated for each subject and then categorised into risk classes (I to V). Another study investigated the ability of the Framingham prediction equation to predict 5 year and 10 year risk of cardiac events (myocardial infarction and fatal coronary heart disease) in people with CKD from the pooled ARIC and CHS studies (N=934). Manual checking of medical records identified only 4 additional cases of CKD missed by the computer search. The recording of a renal diagnosis improved as renal function declined. Only 270/1313 (20%) of people with diabetes, hypertension, and eGFR <60 ml/min/1. In people with stage 3–5 CKD without diabetes and a PCR <100, the percentage of systolic blood pressure measurements in target range increased significantly after 9 months of the DMP (37. In people with stage 3–5 CKD, with diabetes or a PCR >100, there were NS differences in blood pressure measurements in target range at baseline compared to after 9 months on the DMP. This was also true for people with eGFR fall ≥5 ml/min/1. After introduction of a referral assessment service, the referral rate decreased rapidly and by 6 months, an average of five new CKD stage 4 or 5 patients were being referred (0. This referral rate was within the capacity of local nephrology services. In both the derivation (N=6789) and validation cohorts (N=3395), people in the Class V risk index had triple the risk of rapid renal disease progression compared with people in the Class I risk index. The Framingham equation correctly identified men with CKD who would develop a cardiac event within 10 years only 184 15 Information needs 60% of the time, compared with 69% of the time in the non-CKD male cohort and 73% in the original Framingham cohort. In women with CKD, discrimination was 73% for 10-year cardiac events compared with 76% in the original Framingham cohort. The 5-year calibration for men was poor (chi-square 33. The Framingham equation under-predicted cardiac events in women with CKD and had poor 5- and 10-year calibration. Recalibrated models performed better, although prediction remained poor in men with CKD. In women with CKD, re-calibration showed NS difference in predicted and observed cardiac events in 5- and 10-year probability models. It was also prior to the introduction of appropriate Read Codes and the renal NSF. All of these factors may have subsequently improved the identification of CKD in primary care populations. Nevertheless the GDG agreed that it was still possible that people with an abnormal GFR or proteinuria were not classified as having CKD. As this information is usually recorded on practice computer databases it appears that it would be quite simple to devise programmes to identify these people. The introduction of a disease management programme tailored to people with CKD resulted in significant improvements in blood pressure and lipid control. A significant reduction in progression of CKD also followed the introduction of the disease management programme. The GDG were surprised that the tool for predicting rapid decline in kidney function did not include known factors such as hypertension and proteinuria in the score whilst anti-emetic use was.

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The role of the latter effect Angiotensin I Angiotensin Bradykinin converting on renal perfusion pressure is not clear cheap zenegra 100 mg free shipping, A discount zenegra 100 mg on-line. W hen renal per- Potentiation of sympathetic activity fusion drops best 100 mg zenegra, renin is released into the plas- m a and lym ph by the juxtaglom erular cells Increased Ca2+ current Prostaglandins of the kidneys. Renin cleaves angiotensino- gen to form angiotensin I, which is cleaved further by converting enzym e to form Cough? Angiotensin II partici- pates in glom erular filtration rate regulation in a least two ways. First, angiotensin II FIGURE 11-16 increases arterial pressure— directly and Soon after the release of this useful class of antihypertensive drugs, the syndrom e of func- acutely by causing vasoconstriction and tional acute renal insufficiency was described as a class effect. This phenom enon was first m ore “chronically” by increasing body fluid observed in patients with renal artery stenosis, particularly when the entire renal m ass was volum es through stim ulation of renal sodi- affected, as in bilateral renal artery stenosis or in renal transplants with stenosis to a soli- um retention; directly through an effect on tary kidney. Acute renal dysfunction appears to be related to loss of postglom erular the tubules, as well as by stim ulating thirst (Continued on next page) 11. Normal condition depletion as during diuretic therapy, con- Autoregulation gestive heart failure, cirrhosis, and +– +– nephrotic syndrom e. W hen activated, this Afferent Efferent reninangiotensin system plays an im por- arteriole Glomerulus arteriole tant role in the m aintenance of glom erular pressure and filtration through preferen- M yogenic reflex (Laplace) tial angiotensin II–m ediated constriction Tubuloglomerular feedback of the efferent arteriole. Thus, under such Tubule conditions the kidney becom es sensitive B2. Perfusion pressure reduced to the effects of blockade of the renin- but still within autoregulatory range PGE2 (congestive heart failure, angiotensin system by angiotensin I–con- – renal artery stenosis, verting enzym e inhibitor or angiotensin II diuretic therapy, receptor antagonist. Perfusion pressure com prom ised renal function and congestive seriously reduced PGE2 heart failure, the incidence of serious (prerenal azotemia) – changes in serum creatinine during ACE Intra- glomerular inhibition depends on the severity of the pressure pretreatm ent heart failure and renal failure. Second, angiotensin II preferentially constricts the efferent am ong the appropriate m easures for arteriole, thus helping to preserve glom erular capillary hydrostatic pressure and, conse- patients at risk. Acute interstitial nephritis associated with W hen arterial pressure or body fluid volum es are sensed as subnorm al, the renin- angiotensin I–converting enzym e inhibition angiotensin system is activated and plasm a renin activity and angiotensin II levels has been described. This m ay occur in the context of clinical settings such as renal artery stenosis, O pie; with perm ission. M ost of the renal abnorm alities encountered clinically as a result of N SAIDs can be attributed to the action of these com pounds on prostaglandin production in the kidney. Renal vasoconstriction Sodium chloride and water retention are the m ost com m on side ↓Renal function effects of N SAIDs. This should not be considered drug toxicity because it represents a m odification of a physiologic control "Normalized" renal function m echanism without the production of a true functional disorder in the kidney. Inhibition – – by NSAID Compensatory vasodilation induced by renal prostaglandin synthesis Renal Injury Due To Environmental Toxins, Drugs, and Contrast Agents 11. N SAIDs can induce acute renal decom pensation in patients with various renal and extrarenal clinical conditions that cause a decrease in blood perfu- Severe heart disease (congestive heart failure) sion to the kidney. Renal prostaglandins play an im portant Severe liver disease (cirrhosis) role in the m aintenance of hom eostasis in these patients, so disrup- tion of counter-regulatory m echanism s can produce clinically Nephrotic syndrome (low oncotic pressure) im portant, and even severe, deterioration in renal function. Chronic renal disease Age 80 years or older Protracted dehydration (several days) FIGURE11-19 Physiologic stimulus Inflammatory stimuli Inhibition by nonsteroidal anti-inflam m atory drugs (N SAIDs) on pathways of cyclo-oxygenase (CO X) and prostaglandin synthesis Inhibition - by NSAID -. The recent dem onstration of the existence of functionally dis- tinct isoform s of the cox enzym e has m ajor clinical significance, as COX-1 it now appears that one form of cox is operative in the gastric COX-2 constitutive inducible m ucosa and kidney for prostaglandin generation (CO X-1) whereas Stomach Kidney Inflammatory sites an inducible and functionally distinct form of cox is operative in Intestine Platelets (macrophages, the production of prostaglandins in the sites of inflam m ation and Endothelium synoviocytes) pain (CO X-2). The clinical therapeutic consequence is that an N SAID with inhibitory effects dom inantly or exclusively upon the - cox isoenzym e induced at a site of inflam m ation m ay produce the PGE2 TxA2 PGI2 Inflamma- Proteases O2 tory PGs desired therapeutic effects without the hazards of deleterious effects on the kidneys or gastrointestinal tract. A focal diffuse inflam m atory infiltrate Renal Syndrome Mechanism Risk Factors Prevention/Treatment can be found around the proxim al and dis- Sodium retension ↓ Prostaglandin NSAID therapy (most Stop NSAID tal tubules. The infiltrate consists prim arily and edema common side effect) of cytotoxic T lym phocytes but also con- Hyperkalemia ↓ Prostaglandin Renal disease Stop NSAID tains other T cells, som e B cells, and plasm a ↓ Potassium to Heart failure Avoid use in high-risk patients cells. Changes in the glom eruli are m inim al distal tubule Diabetes and resem ble those of classic m inim al- ↓ Aldosterone/renin- Multiple myeloma change glom erulonephritis with m arked angiotensin Potassium therapy epithelial foot process fusion. Potassium-sparing H yperkalem ia, an unusual com plication diuretic of N SAIDs, is m ore likely to occur in Stop NSAID Acute deterioration of ↓ Prostaglandin and Liver disease patients with pre-existing renal im pairm ent, Avoid use in high-risk patients renal function disruption of Renal disease cardiac failure, diabetes, or m ultiple m yelo- hemodynamic bal- m a or in those taking potassium supple- Heart failure ance m ents, potassium -sparing diuretic therapy, Dehydration Stop NSAID or intercurrent use of an angiotensin-con- Old age Dialysis and steroids (? The m echanism of Nephrotic syndrome with: ↑ Lymphocyte recruit- Fenoprofen Stop NSAID N SAID hyperkalem ia— suppression of Interstitial nephritis ment and activation prostaglandin-m ediated renin release— leads Avoid long-term Papillary necrosis Direct toxicity Combination aspirin analgesic use to a state of hyporeninem ic hypoaldostero- and acetaminophen nism. In addition, N SAIDs, particularly abuse indom ethacin, m ay have a direct effect on cellular uptake of potassium. The renal saluretic response to loop diuretics is partially a consequence of FIGURE 11-20 intrarenal prostaglandin production. This Summary of effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on renal function. Characteristically, the histology of this form of N SAID–induced nephrotic syndrom e Thus, concurrent use of an N SAID m ay consists of m inim al-change glom erulonephritis with tubulointerstitial nephritis. This is an blunt the diuresis induced by loop diuretics. Contrast M edium–Associated Nephrotoxicity FIGURE 11-21 RISK FACTORS THAT PREDISPOSE TO CONTRAST Risk factors that predispose to contrast-associated nephropathy. In ASSOCIATED NEPHROPATHY random populations undergoing radiocontrast imaging the incidence of contrasts associated nephropathy defined by a change in serum creatinine of more than 0. For confirmed high-risk patients (baseline serum creatinine values greater than 1. In addition, there are suspected risk factors Diabetic nephropathy Generalized atherosclerosis Diabetes without that should be taken into consideration when considering the value Severe congestive Abnormal liver nephropathy of contrast-enhanced imaging. The initial glom erular vasoconstriction that follows the injection of radiocontrast m edium induces the ↑Endothelin Systemic ↓ATPase liberation of both vasoconstrictor (endothelin, vasopressin) and ↑PGE2 ↑Vasopressin hypoxemia ↑ANF ↑Adenosine Osmotic load vasodilator (prostaglandin E2 [PGE2], adenosine, atrionatiuretic ↑Blood viscosity to distal tubule ↓PGI factor ) substances. The net effect is reduced oxygen deliv- 2 ery to tubule cells, especially those in the thick ascending lim b of H enle. Because of the system ic hypoxem ia, raised blood vis- ↑RBF ↓↓RBF cosity, inhibition of sodium -potassium –activated ATPase and the – increased osm otic load to the distal tubule at a tim e of reduced Calcium oxygen delivery, the dem and for oxygen increases, resulting in antagonists cellular hypoxia and, eventually cell death. Additional factors Theophylline Net ↓O2 delivery Net ↑O2 consumption that contribute to the acute renal dysfunction of contrast-associ- ated nephropathy are the tubule obstruction that results from increased secretion of Tam m -H orsfall proteins and the liberation of reactive oxygen species and lipid peroxidation that accom pa- Cell injury ny cell death. As noted in the figure, calcium antagonists and theophylline (adenosine receptor antagonist) are thought to ↑TH protein ↑Intrarenal number act to dim inish the degree of vasoconstriction induced by con- of macrophages, T cells trast m edium. Stimulation of mesangium The clinical presentation of contrast-associated nephropathy involves an asym ptom atic increase in serum creatinine within 24 Tubular obstruction Superoxidase hours of a radiographic im aging study using contrast m edium , – – dismutase with or without oliguria.