Supportive & Conservative Therapy

The contract between this chapter and the reader.

1. 1. Explain the role of supportive therapy across all glomerular disease.
2. 2. Use RAAS blockade as the foundation.
3. 3. Use SGLT2 inhibitors for proteinuric CKD.
4. 4. Apply blood-pressure and proteinuria targets.
5. 5. Manage edema, thrombosis, and the nephrotic complications.
6. 6. Reduce cardiovascular risk and address lifestyle.
7. 7. Monitor the targets and the expected SGLT2 GFR dip.
8. 8. Recognise when to move to conservative kidney-failure care.
9. 9. Appraise the evidence for the supportive pillars.

A sixty-second reading. Each bullet stands alone.

• Every glomerular disease shares a non-immunosuppressive supportive backbone that slows progression.
• Supportive therapy is given alongside, or instead of, disease-specific immunosuppression.
• RAAS blockade reduces intraglomerular pressure and proteinuria and is the foundation.
• SGLT2 inhibitors are now foundational for proteinuric CKD, diabetic and non-diabetic.
• An early, reversible GFR dip on starting an SGLT2 inhibitor is expected and not a reason to stop.
• Blood pressure is treated to target, lower when proteinuria is present.
• Proteinuria reduction is the therapeutic target and the surrogate for slower progression.
• The nephrotic state is managed for edema, thrombosis, hyperlipidemia, and infection risk.
• The nephrotic state is hypercoagulable, with the highest thrombosis risk in membranous nephropathy.
• Cardiovascular risk reduction and lifestyle measures are part of care.
• Nephrotoxins such as NSAIDs are avoided.
• Targets, electrolytes (potassium), and GFR trajectory are monitored.
• When progression is advanced, conservative kidney-failure management is considered.

The medical core. An expert should agree supportive and conservative therapy is fully covered here.

Why it matters at the bedside

Every chapter in this volume has leaned on this one. Whatever the immune mechanism — or whether there is one at all — the kidney benefits from the same disease-agnostic backbone: lower the intraglomerular pressure, cut the proteinuria, control the blood pressure, manage the nephrotic complications, and reduce cardiovascular risk. For non-immune disease this backbone is the treatment; for everyone it does as much quiet good as the immunosuppression in the spotlight.

Supportive therapy as a universal backbone

• Supportive therapy is the non-immunosuppressive care given to every patient with glomerular disease, alongside disease-specific immunosuppression where that applies, and as the whole of treatment where it does not (diabetic kidney disease, amyloid). Its goals are to slow progression and manage complications, and it is genuinely disease-modifying — not a holding measure. ‘Supportive’ does not mean ‘doing nothing’.

RAAS blockade: the foundation

• Renin-angiotensin-aldosterone system blockade (an ACE inhibitor or ARB) is the foundation. By dilating the efferent arteriole it lowers intraglomerular pressure, which reduces proteinuria and slows progression — the central hemodynamic lever of the first chapter put to therapeutic use. It is given to essentially all patients with proteinuria, as a single agent (the two classes are not combined, since dual blockade adds harm without benefit).

SGLT2 inhibitors

• SGLT2 inhibitors have become foundational for proteinuric chronic kidney disease — diabetic and non-diabetic alike — conferring both kidney and cardiovascular protection (the DAPA-CKD and EMPA-KIDNEY trials). A crucial practical point: starting one causes an early, modest, reversible dip in GFR (the same hemodynamic effect as RAAS blockade), which is expected and is not a reason to stop the drug. They are now part of the default regimen, not an add-on afterthought.

Finerenone and blood-pressure control

• Two further levers complete the progression-slowing core. Finerenone, a nonsteroidal mineralocorticoid-receptor antagonist, reduces residual risk in diabetic CKD (and is emerging more broadly) when layered on RAAS and SGLT2 therapy. And blood pressure is controlled to target — lower when proteinuria is present — because hypertension both reflects and accelerates glomerular injury.

Proteinuria as the target

• Across glomerular disease, proteinuria is both the therapeutic target and the surrogate for outcome: the more it is reduced, the slower the progression. Every supportive lever — RAAS, SGLT2, finerenone, blood-pressure control — is titrated against it, and a falling proteinuria is the signal that treatment is working. It is the number to chase, and the thread that runs through every disease chapter.

Managing the nephrotic state

• The nephrotic state brings its own cluster of problems to manage: oedema (salt restriction and diuretics, a loop diuretic with a thiazide added if needed); a hypercoagulable, thrombosis-prone state (highest in membranous, anticoagulation when the risk is high, as the albumin falls); hyperlipidemia (a statin); and an infection risk from immunoglobulin loss (vaccination and vigilance). These run in parallel with whatever treats the underlying disease.

Cardiovascular risk and lifestyle

• Chronic kidney disease is a cardiovascular risk state, so cardiovascular risk reduction is integral: a statin, blood-pressure control, and lifestyle measures (weight, smoking cessation). Nephrotoxins — NSAIDs above all — are avoided, and dietary measures (moderate sodium and protein, the renal diet as CKD advances) support the regimen. The kidney is treated in the context of the whole cardiovascular-renal patient.

Targets and monitoring

• Success is monitored against targets: proteinuria (reduction), blood pressure (to target), and the eGFR trajectory — distinguishing the expected early SGLT2/RAAS dip from genuine decline. Potassium is monitored on RAAS and mineralocorticoid-antagonist therapy, and the nephrotic complications (thrombosis, infection) are watched for. Monitoring closes the loop between the supportive levers and the outcome they aim at.

Conservative kidney-failure care

• When progression is advanced and irreversible, the supportive role broadens into conservative kidney-failure management: advance care planning, symptom control, and preparation for kidney replacement therapy — or, where chosen, conservative (non-dialytic) care as a legitimate path. Supportive therapy thus spans the whole arc, from slowing early disease to caring for the patient whose kidneys are failing.

The evidence and the SGLT2 era

• The evidence base has been transformed in a few years. RAAS blockade has long-established antiproteinuric and renoprotective benefit; SGLT2 inhibitors now protect the kidney and heart across proteinuric CKD (DAPA-CKD, EMPA-KIDNEY); finerenone reduces progression and cardiovascular events; and statins reduce cardiovascular risk in CKD. Proteinuria is the validated, modifiable surrogate that ties them together. The contested edges — how low to push proteinuria and blood pressure, the threshold to anticoagulate — are matters of judgement layered on a strong foundation.

Five fully-built tables.

Table A — The supportive backbone

Table B — The progression-slowing pillars

Table C — Managing the nephrotic state

Table D — Targets and monitoring

Table E — CV risk, lifestyle, and conservative care

Visualise & Map

Numbered rules. These numbers are the cross-reference handle for the cases and flowcharts.

Clinical Reasoning

Five cases. Each stops you at a decision before it answers it.

Exhaustive. Every rule in the chapter is here.

Safety & Evidence

Panel A — Red flags

Panel B — NEVER DO

Anti-patterns clinicians fall into. Each becomes a Level 22 distractor.

The grade reflects strength of evidence, not importance.

Patient Decisions

Outcomes as natural frequencies. Figures are representative; the direction of effect is given where precise numbers are uncertain.

Apply & Test

Copy-paste chart notes that map to the real decisions in this chapter.

Template 1 — Supportive-therapy plan note

• RAAS blockade (single agent; no dual block): ___.
• SGLT2 inhibitor started (proteinuric CKD); early GFR dip expected: ___.
• Finerenone for residual risk (if applicable): ___.
• Blood-pressure target; proteinuria target: ___.
• CV risk (statin), lifestyle, nephrotoxins avoided: ___.

Template 2 — Nephrotic-state / monitoring note

• Edema (salt/diuretics); hyperlipidemia (statin); infection risk: ___.
• Thrombosis risk (albumin; membranous); anticoagulation decision: ___.
• Monitoring: proteinuria, BP, eGFR trajectory, potassium: ___.
• Distinguish expected SGLT2/RAAS dip from genuine decline: ___.
• Conservative care / RRT planning if advanced: ___.

Pre-rounds compression. Rules only.

Active recall. At least one card per objective.

Micro-teaching for rounds. Two scenarios, five steps each.

Metacognition anchored to this chapter's tensions. No answers provided.

1. 1. Proteinuria is the surrogate we chase, but how low is low enough — and when does pushing further trade benefit for adverse effects?
2. 2. The nephrotic thrombosis risk is real but so is the bleeding risk of anticoagulation; where do you set the albumin threshold to anticoagulate?
3. 3. Four renoprotective levers each add benefit and burden; how do you decide how high to build the stack for a given patient?
4. 4. Hyperkalemia tempts clinicians to drop renoprotective drugs; how do you weigh keeping a beneficial drug against the safety of the potassium?
5. 5. When does the goal shift from slowing progression to conservative, symptom-focused care — and who should make that call?

Nine items, each anchored in this chapter. At least one per objective.